Is "Why Evolution Is True" True: Coyne's Model For Discrediting Darwin's Thepry

Post 35: Darwinism As Science-Alternative Perspective

2011-02-10T08:49:00.000-08:00

Post 34 initiated the evaluation of WEiT’s position that the central tenents of Darwinism have been verified by as demonstrated by several lines of evidence.

One line of “evidence” involved WEiT’s descriptions of causal condations that presumably resulted in changes between major morphological forms.

As concluded in that post, WEiT’s explanations were based on terms that represent speculation rather than observations obtained by experimental testing (as specified by WEiT and Fitzhugh below), and thus, by the book’s own science criteria, do not suffice as plausible test evidence.

Thus this line of "evidence" can be ruled out as providing support that Darwinism’s tenents have been verified.

The second line of evidence involved examples of “fulfilled predictions” that, in one way or another, were based on the prediction of the discovery of new organisms whose morphological traits would be sufficiently similar to the previously documented assumed transitional-form sequences (in both extinct and extant organisms) to be interpreted as a trait (organism) in the originally documented sequence.

WEiT states that there are two "kinds" of evidence that verifies Darwinism, the first specified in the following:

So how do we test evolutionary theory — . There are actually two kinds of evidence. The first comes from using the six tenents of Darwinism to make testable predictions. By predictions, I don’t mean that Darwinism can predict how things will evolve in the future. Rather, it predicts what we should find in living or ancient species when we study them. Here are some evolutionary predictions. (page 17) [emphasis supplied]

Following this perception of testing evolutionary theory with predictions, WEiT lists the first "kind" of predictions (that should be associated with the book’s six Darwinism tenents) summarized as follows by their principle concepts (pages 18 & 19).

— change in the fossil record;
— species dividing into two or more;
— species that link together major groups os suspected common ancestry;
— species that show genetic variation for many traits;
— cases of imperfect adaptation;
— see natural selection acting in the wild.

The goal for this post is to examine the plausibility of "evidence," presented by WEiT as “fulfilled predictions,” that were derived according to the following analytical sequence, which describe the general procedure utilized in the book’s prediction examples.

1. A series of known fossil organisms or organism traits are presented as a sequence of diversification of morphological forms.

2. It is predicted that additional fossil organisms will be discovered that exhibit enough morphological similarities between two forms in the known sequence to be judged as intermediate organisms in the sequence.

3. Such an organism is discovered.

4. Thus, the prediction is fulfilled, with some sort of implied application to Darwinism’s verification.

This analysis structure is essentially a summarization of a professional paper by Fitzhugh (86) that thoroughly describes why such a prediction procedure results in “failed evidence.”

It is Fitzhugh's "failed evidence" concept that relates to Post 34 closed with the following:

Did WEiT, knowingly or unknowingly, commit a cardinal scientific error in the nature of a “syllogistic faux-naif?”

Basically, a syllogism is a method for arranging required components of an argument in a diagrammatic structure that insures the inclusion of required statements on which to base the argument and to help insure the arguments conclusion has conformed to several basic principles of logic.

It is the syllogism structure and logic that, in this post, is used to evaluate WEiT’s prediction examples.

One of the major “fulfilled predictions” addressed by WEiT involved the fossil Tiktaalik roseae:

One of the greatest fulfilled predictions of evolutionary biology — a transitional form between fish and amphibians. This is the fossil species Tiktaalik roseae —. (pages 35-38) [underlining substituted for original italicized text-other emphasis supplied]

Accompanying the discussion of a number of morphological traits that proved the fossil was a transitional form in its proper setting, WEiT stated:

Its discovery is a stunning vindication of the theory of evolution. (page 35) [emphasis supplied]

And:

— the most tangible evidence that evolution was true. (page 38) [emphasis supplied]

In short, this fossil was presented by WEiT as a sort of “poster child” as an example of the predictive successes of “Darwinian science.”

The logic literature abounds with treatments of syllogistic-styled arguments, but Fitzhugh’s paper is particularly relevant to the thrust of this post since Tiktaalik roseae was also the organism that Fitzhugh used as a “real world” example to support a more formal discussion fundamentally involving the differences between evidence and inference in evolutionary biology prediction efforts.

It is something of an understatement that Fitzhugh’s paper is “tedious” and by no means a subject for causal perusal, perhaps why it so seldom referenced in evolutionary biology literature, although other reasons will likely become apparent as WEiT’s view of fossil evidence (and presumably representing evolutionary biology's views) comes under the scrutiny of Fitzhugh’s paper.

Syllogistic-arranged logic is, as stated above, tedious to follow since the logic flow involves a tight sequence that requires more than a casual reading to fully comprehend the sequence.

Fitzhugh incorporates his analysis of “predictions,” based on the “recursive” use of observed phenomena to predict aspects of the same phenomena, within the logic of hypothesis and theory testing, thereby addressing WEiT’s requirement of testing as an integral requirement for determining the validity of scientific theories.

A contrary view of this post’s condemnation of WEiT’s supportive evidence for Darwinism’s validity must also be contrary to Fitzhugh’s syllogism-based explanations of hypothesis and theory testing --- that is the challenge for "skeptics" as addressed below.

Thus, a close reading of his syllogism examples, admittedly something of a challenge, must be the basis for such skepticism.

One subtle aspect of Fitzhugh’s treatment of ‘potential” versus “actual” hypothesis and theory testing (refer to the following summary of syllogism (14)) is the implications that the whole Darwinian process has no predictable power concerning the development of morphological diversity, which is acknowledged by WEiT by the following:

By predictions, I don’t mean that Darwinism can predict how things will evolve in the future. (page 17) [emphasis supplied]

If such be the case, then as discussed by Fitzhugh under the rules of logic, as described below in syllogism (14), expecting a definitive prediction of Tiktaalik’s morphological traits would fall under the same problem of impossibility, considering that, although not a “future” development, it would qualify as such because it is new and “future” forms are new.

When distilled to its fundamental concept, Fitzhugh’s paper points out the critical difference between evidence and inference, and as such, provides the rationale for determining that WEiT’s transitional sequence “fulfilled predictions” do not qualify as evidence that verify’s Darwinian tenents but rather are inferences that have not been tested.

Fitzhugh's syllogism sequence begins with an example that illustrates why WEiT's evidence of "predictions fulfilled" cannot be adapted to a correctly constructed syllogism-styled prediction, and ends with an example of why an actual syllogism test of prediction based on correctly applied evidence, versus a potential syllogism test prediction, cannot be realistically performed.

Although paraphrasing or otherwise “explaining” or shortening his explanations would run the danger of creating misinterpretations, for those who are not inclined to delve into the particulars, the following summary of Fitzhigh's five syllogisms (and associated text) are offered.

If this "brief" of Fitzhugh's thoroughly discussed syllogisms is sufficient for the reader, at least as an inirtial introduction, the reader may wish to skip to Fitzhugh's discussion following syllogism (14) and this post's ending summary --- skip the gritty details that Fitzhugh uses to justify his conclusion in syllogism (14).

But should details be desired,his entire text involving Tiktaalik directly and his “contrived” example representing a Tiktaalik-type prediction, starting with the section labeled "Failed Evidence For Evolution," is presented complete as in Fitzhugh’s paper (with bold emphasis supplied).

Fitzhugh's syllogism sequence begins with syllogism (11) as an example that illustrates why WEiT's observations do not constitute valid predictions and ends with syllogism (14) as an example that illustrates why a syllogism structured prediction cannot be assembled for a true prediction test.

Syllogism (11) is the analytical form representing an “abductive” line of logic designed from a body of “Tiktaalik type” observations, with a confirmed hypothesis designed to verify the concept of natural selection.

Fitzhugh essentially states that the syllogism’s argument is insufficient to validate the hypothesis because it is “deductive,” (proceeds from a general observation to specifuic entities) and thus requires a different argument sequence as in syllogism (12a)

Syllogism (12a) essentially arranges the syllogism (11) information in a different argument order that adds a “predicted test consequence”, i.e., prediction of what new fossil will be found.

Fitzhugh explains that the syllogism’s deduction of test consequences is inadequate because nothing in the syllogism concerns statements of specific traits to be exhibited by the newly discovered fossil, i.e., the new fossil could exhibit any possible combination of traits.

Thus, new fossil forms are just new effects that need to be explained and thus cannot qualify as test evidence, thus requiring an additional change in the argument sequence, as in syllogism (12b).

Syllogism (12b), which is only illustrated with the new phrasing of the “predicted test consequences,” incorporates the specific traits that should characterize a newly discovered fossil for validation of the theory.

But this argument sequence is also invalid for reasons best left to Fitzhugh’s explanations, which leads to syllogism (13).

Syllogism (13) starts to more directly address why fossils such as Tiktaalik represent evidence to which a theory would be applied rather than evidence that could assess the theory’s validity.

Fitzhugh points out that the inadequacy of this syllogism’s argument lies in the lack of causal conditions descriptions in the syllogism’s premises—causal conditions that would need to be witnessed from which the tests consequences should be deducible.

These causal conditions to be witnessed are present conditions (rather than past conditions as in syllogisms (11), (12a), and (12b) which cannot be observed), and thus fossil evidence is ruled out which leaves future conditions to provide test results as added in syllogism (14).

Syllogism (14), which Fitzhugh introduces as potential test evidence, incorporates the essential element of an observed causal condition that points to what might be interpreted as “the” fatal logic error in WEiT’s “predictions fulfilled” examples and likely evolutionary biology’s insurmountable problem for validating Darwinism’s tenents — the syllogism argument specifies “Potential Test Consequences” as “occurrences of the trait should increase in the population into the future.”

The critical emphasis is on "Potential Test Consequences" that depend on "future observations" which eliminate the syllogism from consideration that it represents an argument for a test that will actually be performed.

Failed Evidence For Evolution [bold and underlining supplied throughout Fitzhugh’s text]

The most consistent point of view regarding the testing of either a theory in evolutionary biology or a phylogenetic hypothesis has been that predictions of particular organisms, or their characters, qualify as relevant test evidence (e.g. Wiley 1975; Barnosky and Kraatz 2007; Prothero 2007; contra Fitzhugh 2006a, 2008a). In other words, the same class of evidence that is used to infer hypotheses, as well as a theory such as natural selection, also stands as supporting evidence. A good example of this position is the discovery of ‘transitional forms’ in the fossil record. Consider the recent description of Tiktaalik roseae by Daeschler et al. (2006; see also Shubin et al. 2006), a fossil of a Devonian fish with pectoral fins intermediate in form between fins and limbs. In commenting on this find, Ahlberg and Clack (2006: 748) regard the fossil as significant because “it demonstrates the predictive capacity of palaeontology.” Similarly, T. roseae was cited in chapter one of the publication, Science, Evolution, and Creationism (National Academy of Sciences and Institute of Medicine 2008: 1, 3; see also Ayala 2006), within the section entitled, “The scientific evidence supporting biological evolution continues to grow at a rapid pace.” Using this species as their example, it is claimed that,

“A prediction from more than a century of findings from evolutionary biology suggests that one of the early species that emerged from the Earth’s oceans about 375 million years ago was the ancestor of amphibians, reptiles, dinosaurs, birds, and mammals. The discovery of Tiktaalik strongly supports that prediction. Indeed, the major bones in our own arms and legs are similar in overall configuration to those of Tiktaalik.

The discovery of Tiktaalik, while critically important for confirming predictions of evolution theory, is just one example of the many findings made every year that add depth and breadth to the scientific understanding of biological evolution.”

Is this fossil confirming evidence for “evolution theory?” Unfortunately, the answer is no. Tiktaalik roseae provides neither confirming evidence for an evolutionary transition from fishes to terrestrial tetrapods nor support for any of the theories within evolutionary biology. The following contrived example can make this evident.

Fitzhugh then demonstrates a general parallel with the Tiktaalik prediction with the following simple set of “contrived” fossil traits in the following illustration, which information is then analyzed in several syllogisms.

The fundamental goal of these syllogisms and associated discussions is to clearly draw a distinction between inference and evidence.

The illustration’s form D would represent the Tiktaalik fossil. The following Fitzhugh text format is listed in separated sentence-by-sentence sequence to perhaps more clearly illustrate the sequence logic.

A series of fossils are found from the dated strata shown in Figure 1A.

The oldest fossils are of individuals lacking lateral appendages or dorsal ornamentation,

whereas slightly younger fossils show the presence of one pair of appendages, and

individuals from the youngest strata have three pairs.

As well, members of the two youngest species have varying degrees of dorsal ornamentation.

But, there is a gap in the record, between 165 and 100 mya where no members of this group had been found thus far.

The phylogenetic hypothesis for these fossils (Fig. 1B) suggests the following two transformation series:

(a) absence of appendages ! [form a-us]

one pair of appendages ! [form b-us]

three pairs of appendages, [form c-us] and

(b) smooth dorsal margin ! [forms a-us and b-us]

one pair of dorsolateral protuberances ! [form c-us]

a row of five protuberances over the dorsum. [form d-us]

The actual inference of these hypotheses from the observations would have the following abductive form (cf. Fitzhugh 2005a, b, 2006a, b, 2008a, b, in press):

[11] Theory:
“descent with modification’ – if character x(0) exists among individuals of a reproductively isolated, gonochoristic or cross-fertilizing hermaphroditic population, and character x(1) originates by mechanisms a, b, c... n, and becomes fixed within the population by mechanisms d, e, f... n [= ancestral species hypothesis], followed by event or events g, h, i... n, wherein the population is divided into two or more reproductively isolated populations, then individuals to which descendant species hypotheses refer would exhibit x(1)

Observations (Fig. 1A):
(1) individuals to which species hypotheses b-us, c-us, and d-us refer have appendages in contrast to a convex ventrum as seen among individuals to which other species hypotheses refer;
(2) individuals to which species hypotheses c-us and d-us refer have dorsal protuberances in contrast to a convex dorsum as seen among individuals to which other species hypotheses refer
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Hypothesis (Fig. 1B):
(a-us (b-us (c-us d-us))), i.e.,
(1) ventral appendages originated by some unspecified mechanism(s) within a reproductively isolated population of individuals with a convex ventrum, and the condition became fixed in the population by some unspecified mechanism(s), followed by an unspecified event(s) that resulted in two reproductively isolated populations, i.e. members of species a-us and members of an ancestral species eventually leading to members of b-us, c-us, and d-us;
(2) dorsal protuberances originated by some unspecified mechanism(s) within a reproductively isolated population of individuals with a convex dorsum, and the condition became fixed in the population by some unspecified mechanism(s), followed by an unspecified event(s) that resulted in two reproductively isolated populations, i.e. members of species c-us and d-us.”

From the temporal distribution (Fig. 1A) and phylogenetic hypothesis (Fig. 1B), one might claim that specimens will be found in the 165 to 100 mya strata that exhibit appendages and dorsal surface features that are transitional to what has been found in earlier and later strata (Fig. 1C). Such a prediction, if found to be the case, would be claimed to provide notable evidential support for the phylogenetic hypothesis, and by extension the ability of evolutionary biology to steer us in the right direction when it comes to seeking ‘transitional forms.’ Upon further investigations of the 165 to 100 mya strata fossils are found, with two pairs of appendages and three dorsal protuberances. Such a finding is in accord with what was ‘predicted.’ But, does this new fossil serve as a legitimate test of the phylogenetic hypothesis? Does the finding increase the veracity of evolutionary biology, at least in the context of, say, natural selection? Let’s first consider the situation if it is the case that fossils are test evidence for the phylogenetic hypothesis in [11] (Fig. 1B). To assert that the discovery of some ‘transitional’ form in strata between 165 and 100 mya supports (a-us (b-us (c-us d-us))), that prediction would have to be a deductive consequence of the form shown in [8]. The deduction would, at a minimum, have the following appearance:

[12a] Theory:
“descent with modification” – if character x(0) exists among individuals of a reproductively isolated, gonochoristic or cross-fertilizing hermaphroditic population and character x(1) originates by mechanisms a, b, c... n, and becomes fixed within the population by mechanisms d, e, f... n [= ancestral species hypothesis], followed by event or events g, h, i... n, wherein the population is divided into two or more reproductively isolated populations, then individuals to which descendant species hypotheses refer would exhibit x(1)

Hypothesis:
(a-us (b-us (c-us d-us))), i.e.,
(1) ventral appendages originated by some unspecified mechanism(s) within a reproductively isolated population of individuals with a convex ventrum, and the condition became fixed in the population by some unspecified mechanism(s), followed by an unspecified event(s) that resulted in two reproductively isolated populations, i.e. members of species a-us and members of an ancestral species eventually leading to members of b-us, c-us, and d-us;
(2) dorsal protuberances originated by some unspecified mechanism(s) within a reproductively isolated population of individuals with a convex dorsum, and the condition became fixed in the population by some unspecified mechanism(s), followed by an unspecified event(s) that resulted in two reproductively isolated populations, i.e. members of species c-us and d-us
------------------------------------------------------------------------------------------------------------------------------------------------------------------
Observations that led to the original inference of the hypothesis (Fig. 1A):
(1) individuals to which species hypotheses b-us through d-us refer have appendages in contrast to a convex ventrum as seen among individuals to which other species hypotheses refer; (2) individuals to which species hypotheses c-us and d-us refer have dorsal protuberances in contrast to a convex dorsum as seen among individuals to which other species hypotheses refer

“Predicted” test consequence, per Figure 1A:
Fossils of a ‘transitional’ form should be found in strata between 165 and 100 mya that have a number of appendages or dorsal protuberances that are intermediate to what are seen among members of species c-us and d-us (cf. Fig. 1C).

What should be noticed in this example is that the deduction is invalid insofar as the conclusion of the ‘predicted’ test consequence is not possible. The premises, especially hypothesis (a-us (bus (c-us d-us))), presents a series of causal conditions that, in conjunction with the theory of ‘descent with modification,’ account for the observed effects originally observed (Fig. 1A). From these premises there are no statements that could be derived that refer to specific properties of unobserved individuals. In point of fact, the premises do not preclude finding new fossils with any possible combination of characters. The consequence is that such fossils, if found, provide no relevant information that could assess the veracity of the hypothesis being tested. Additional fossil forms are simply newly observed effects also in need of explanation. The observations of new individuals cannot qualify as the test evidence for evaluating (a-us (b-us (cus d-us))) (Fitzhugh 2005a, b, 2006a, b, 2008a, b). The only valid statements that could be inferred from the premises in [12a], and would therefore function as potential tests of the hypothesis, would be those regarding effects that are direct and specific consequences of the causal events stated in the hypothesis, e.g.,

[12b] Correct predicted consequences:
Respective effects U, V, W,... n should be observed, indicating the causal events of character origin and fixation of appendages and dorsal protuberances in an ancestral population, and effects X, Y, Z,... n should be observed, indicating occurrences of causal events resulting in splittings of populations into separate, reproductively isolated groups.

Clearly, to speak of the testing of a phylogenetic hypothesis represented as a ‘cladogram’ (Fig. 1B, C) would not be possible given that such branching diagrams do not provide even sufficient specific details of the causal events one would be interested in testing. Inferring potential tests would only be possible once the different classes of events implied by such a diagram are fully explicated and replace the vaguely worded minor premise in [12a].

One of the inherent difficulties with proceeding to the next step of actually testing explanatory hypotheses is that the process can be severely constrained by the amount of time that has elapsed between the hypothesized events to be tested and the observed effects. There is the possibility that the ensuing span of time is sufficient to eliminate the kind of test evidence identified in [12b]. In such a situation, we might say a hypothesis remains ‘potentially testable,’ as opposed to ‘untestable.’ In other words, empirical observations might eventually be available under current conditions. An untestable hypothesis would be one in which the consequences previously deduced are entirely beyond scrutiny because the theory or associated background knowledge upon which it is based, in the form of auxiliary theories, allow for no conceivable conditions under which the consequences can be empirically verified or refuted. Such an instance will be discussed in the next section.

A more general consideration regarding the observations in Figure 1A in terms of ‘evidence’ for any of the theories in evolutionary biology, such as natural selection, genetic drift, etc., suffers the problem just encountered for hypothesis testing. As in the instances described earlier of the fossils of Tiktaalik roseae being regarded as evidence supporting evolution, the failure of this position is that it rests on the evidence to which a theory would be applied, not evidence that could actually assess the theory. From the observations in Figure 1A, for one to claim that new fossils provide supporting evidence for an evolutionary theory, say natural selection, would mean that the deductive argument would have the form,

[13] Natural selection theory:
in the event a novel, heritable character is derived as a consequence of mutation, and this character has a positive influence on fitness, then the character will become progressively prevalent in the population

“Causal” condition:
fossils that are members of a new species should be found in strata between 165 and 100 mya
------------------------------------------------------------------------------------------------------------------------------------------------------------------
“Predicted” consequence:
individuals will exhibit conditions intermediate of those observed in earlier and later individuals.

What is apparent in this instance is that the inference is not valid. The conjunction of the two premises would not allow for the conclusion. More fundamental, the minor premise does not state the proper antecedent conditions from which the theory of natural selection could be subjected to testing (cf. [9]). As theories have the form, ‘given causal condition x, effect y will ensue,’ deducing potential test observations would necessitate that the minor premise state the causal conditions that would need to be witnessed, from which consequences should be deducible if the theory is true. Testing theories proceed from knowing the causal conditions in the present to the subsequent observations of effects. Notice that this condition differs substantially from what was shown in [10] and [12a/b] for hypothesis testing, where causal conditions were past events that cannot be observed, such that what must be obtained is evidence related as specifically as possible to those events. Rather than relying on fossils, which are the effects that have served as evidence for the abductive inferences of evolutionary theories and hypotheses, the proper inference of potential test evidence of the theory of natural selection would have the form,

[14] Natural selection theory:
in the event a novel, heritable character is derived as a consequence of mutation, and this character has a positive influence on fitness, then the character will become progressively prevalent in the population
Causal condition: a new, heritable trait is observed within a population, that potentially enhances relative fitness
------------------------------------------------------------------------------------------------------------------------------------------------------------------
Potential Test consequence:
occurrences of the trait should increase in the population into the future.
The evidential requirements for testing evolutionary hypotheses and theories immediately preclude simply recording the occurrences of fossils or extant organisms. What are observed of organisms are properties that prompt the applications of a variety of theories in evolutionary biology, such that those properties could not recursively assess the explanatory import of the theories and hypotheses abductively applied to them. Far more careful consideration of the nature of test evidence is required.

The general nature of the problem addressed by Fitzhugh is addressed in the following material that constitutes parts of the paper’s introduction and various summarization statements.

The claim by biologists and ID advocates alike that observed effects can serve as ‘evidence’ supporting their alternative views suffers from a fundamental error – that of confusing the ‘evidence’ one uses as the basis for inferring a theory or hypothesis with the ‘evidence’ needed to critically assess either. It is a distinction Hanson (1958: 200, note 2, emphasis original; Achinstein 1970) recognized as too often ignored or denied as a consequence of the adoption of hypothetico-deductivism (H-D). There is,

”...the logical distinction between (1) reasons for accepting an hypothesis H, and (2) reasons for suggesting H in the first place. (1) is pertinent to what makes us say H is true, (2) is pertinent to what makes us say H is plausible. Both are the province of logical inquiry, although H-D theorists discuss only (1) saying that (2) is a matter for psychology or sociology – not logic. This is just an error....

We are discussing the rationale behind the proposal of hypotheses as possible explicantia. H-D theorists never raise the problem at all.”

A common consequence of not clearly acknowledging the logic of hypothesis and theory formation is that the ‘reasons’ in (1) and (2) are not recognized as being very different classes of evidence. Evidence used to infer some theory or hypothesis cannot recursively function as evidence supporting the very theories or hypotheses that have been inferred to account for that evidence. The goal of this paper is to provide a brief outline of how to avoid the common mistake of confusing evidence ‘suggesting’ a particular theory or hypothesis with the evidence for ‘accepting’ that theory or hypothesis. Establishing this distinction has the benefit of reorienting debate about evolution and ID back to the real issue: applying the accepted tenets of testing as the means of deciding the explanatory merits of theories (Sober 1999). This is not a matter of promoting any kind of demarcation criterion between science and non-science. As was suggested by Laudan (1983; see also Stamos 2007), rather than stressing demarcation, which might be a tentative proposition, we should judge claims on the basis of what can be provided in the way of supporting or refuting empirical evidence. As such, careful consideration is required to make the distinction stated by Hanson (1958), especially when comparing evolutionary biology and ID.

Evidence and Inference

Inference involves a relation between evidence and conclusion – evidence comprises the premises from which one infers a conclusion (Salmon 1984b). To speak of the support for a proposition is to refer back to the premises. For instance, in the classic example of deduction, ---.

Evolution and ID Cannot Be Defended Via Abductive Evidence

We can now to assess the popular claims that observed organisms, either extant or as fossil remains, provide evidence supporting any of the theories encompassed by evolutionary biology or ID. Representative arguments found in the evolutionary and ID literature will be examined next.

His “summary” perspectives included the following:

The standard within the various fields of science that allow for critical evaluations of theories and hypotheses is the process of testing.

Since this principle is recognized by WEiT (see opening WEiT quotes in Post 34), a central question is posed:

Do WEiT’s presentations of filfilled predictions satisfy the concept of scientific testing

— the real issue is to identify what evidence can actually be provided for the support of refutation of a theory or hypothesis — to speak of testing means we once again invoke the term “evidence.”

What becomes critical is to recognize how “evidence” plays different roles in the acquisition of understanding. We have to differentiate between evidence that compels us to infer a particular theory or hypothesis from evidence that, in the context of testing, supports or refutes those claims.

— it is the theory (and relevant background knowledge) and effects that provide the basis for the hypothesis provided — . In other words, we have the “reasons for suggesting H in the first place.” These reasons, i.e., evidence, stand entirely separate from the “reasons for accepting ... H —.

In referring to one of the paper’s syllogism illustrations, Fitzhugh comments:

— the inference of potential tests of a theory stipulate conditions having the form of an experiment, where one must put themselves in a position of witnessing the “experimental causal conditions” as well as the subsequent “predicted consequence.” — An important consequence is that the effect(s) that prompted inference of the hypothesis in the first place could not then serve as test evidence of that hypothesis, much less could effects of the same class as those that led to the hypothesis.

This post's conclusions concerning the scientific adequacy of the general structure ofWEiT's myriad of predictions as validation of Darwinism are perhaps most clearly conveyed by:

WEiT's perspective of criteria to which evidence via "prediction" must conform:

For a theory to be considered scientific, it must be testable and make verifiable predictions. That is, we must be able to make observations about the real world that either support it or disprove it. (Page 15) [emphasis supplied]

WEiT's perception of what evidence "prediction" must address:

The theory of natural selection has a big job — the biggest in biology. Its task is to explain how every adaptation evolved, step by step, from traits that preceded it. This includes not just body form and color, but the molecular features that underlie everything. (Page 119) [underlining substituted for the original italicized text-other emphasis supplied]

WEiT's perspective of what evidence "prediction" produces:

---it predicts what we should find in living or ancient species when we study them (page 17)

Within these three requirements, "things" to be explained by prediction include "what we should find" repeated from the second WEiT quote in this post.

— change in the fossil record;

— species dividing into two or more;

— species that link together major groups of suspected common ancestry;

— species that show genetic variation for many traits;

— cases of imperfect adaptation;

— see natural selection acting in the wild.

And the six "components" of Darwinism that WEiT also perceives must also be addressed by these foregoing predictions:

--- evolution, gradualism, speciation, common ancestry, natural selection, and nonselective mechanisms of evolutionary change. (page 3)

The implausibility of other WEiT predictions, designed iafterthe general format of the Tiktaalik example for providing evidence that supports the validation of Darwinism tenents, is demonstrated by evaluating the prediction format under the logic illustrated in Fitzhugh's foregoing syllogisms, particularly syllogism (14).

In short, as stated by Fitzhugh:

But, does this new fossil serve as a legitimate test of the phylogenetic hypothesis? Does the finding increase the veracity of evolutionary biology, at least in the context of, say, natural selection?

--- such fossils, if found, provide no relevant information that could assess the veracity of the hypothesis being tested. Additional fossil forms are simply newly observed effects also in need of explanation.

Tiktaalik roseae provides neither confirming evidence for an evolutionary transition from fishes to terrestrial tetrapods nor support for any of the theories within evolutionary biology.

Since this post only treated a "generic" perspective of WEiT's prediction concepts, the question remains:

How did WEiT use its prediction examples to validate the tenets in its two lists, as summarizeed above?

Literature Cited

Fitzhugh, Kirk. Evidence for Evolution Versus Evidence for Intelligent Desigm: Parallel Confusions. Evolutionary Biology. Volume 37, Numbers 2-3, 1007.

POST 34: Darwinism As Science-WEiT's Perceived Association

2011-01-31T19:04:00.000-08:00

WEiT’s basic premise for the scientific validity of Darwinism is fundamentally expressed in the following:

—when we say that “evolution is true,” what we mean is that the major tenents of Darwinism have been verified. Organisms evolved, they did so gradually, lineages split into different species from common ancestors, and natural selection is the major engine of adaptation. (page 223) [emphasis supplied]

To this foregoing perception the following two implications are offered that clarify WEiT’s basic premise for the validity of a scientific theory:

—a theory of evolution is more than just the statement that “evolution happened”: it is an extensively documented set of principles — I’ve described six major ones — that explain how and why evolution happens. (page 15) [underlining substituted for the original italicized text-other emphasis supplied]

— in science, a theory is much more than just a speculation about how things are: it is a well-thought-out group of propositions meant to explain facts about the real world. (page 15) [emphasis supplied]

The objective of this post is based on WEiT’s perception of the conditions that determine the plausibility of the two foregoing statements impact on the book’s claim that the major tenents of Darwinism have been verified.

For a theory to be considered scientific, it must be testable and make verifiable predictions. That is, we must be able to make observations about the real world that either support it or disprove it. (page 15) [emphasis supplied]

WEiT then provides the particular features that this scientific theory perception applies to:

The theory of natural selection has a big job — the biggest in biology. Its task is to explain how every adaptation evolved, step by step, from traits that preceded it. This includes not just body form and color, but the molecular features that underlie everything. (page 119) [underlining substituted for the original italicized text-other emphasis supplied]

The foregoing quote essentially encapsulates the books’s critical shortcoming treated in this post: that the scientifically plausible how of natural selection must include the scientifically plausible explanation via observed evidence of how body forms develop, i.e., major body forms as expressed by WEiT.

The singular point to establish in this post’s evaluation of WEiT’s arguments, in terms of scientific observations as documentation in support of Darwinism, is that the hypothesis centrally involves the development of different body plans or body forms as recognized in the following:

Of course because the fossil record is incomplete, we can’t expect to document every transition between major forms of life. (page 25) [emphasis supplied]

In several other texts, as in the foregoing quote, WEiT clearly equates body plan diversity with speciation, i.e., WEiT’s development of major species forms, and vice versa:

How does this diversity arise from one ancestral form? This requires the third idea of evolution: that of splitting, or, more accurately, speciation. (page 5) [underlining substituted for the original italicized text-other emphasis supplied]

What we’re asking about here in not whether speciation happens, but how. — The glacial pace of speciation means that, with a few exceptions, we can’t expect to witness the whole process, or even a small part of it, over a human lifetime. To study how species form, we must resort to indirect methods, testing predictions derived from the theory of geographic speciation. (page 178) [emphasis supplied]

— perhaps the most striking fact about nature is that it is discontinuous. When you look at animals and plants, each individual almost always falls into one of many discrete groups. — These discrete clusters are known as species. — How these groups arise is the problem of speciation — or the origin of species. (page 169) [underlining substituted for the original italicized text-other emphasis supplied]

We may never have enough information to reconstruct the evolution of many traits or even, in extinct species, to understand precisely how those traits functioned. (page 120) [emphasis supplied]

The essence of the foregoing WEiT observations are appropriately summarized in one critical statement among the book’s perspectives:

If we want to explain biodiversity — we must also explain how new species arise. (page 170) [underlining substituted for original italicized text-other emphasis supplied]

and furthermore:

— we finally have a reasonably complete picture of what species are and how they arise. And we also have evidence for that process. (page 170) [emphasis supplied]

In the foregoing quotes, the concept to be stressed is the requirement to explain how species, i.e. major body plans, diversified.

Thus, there are two essential questions to be posed for the book’s perceptions of evidence that satisfies scientific criteria:

1. What does WEiT offer that can be reasonably interpreted as “scientific” evidence?

2. What does WEiT offer that can be reasonably interpreted as speculation ?

In closing the book’s Chapter 5, “The Engine of Evolution,” there occurs the following:

The obvious conclusion: we can provisionally assume that natural selection is the cause of all adaptive evolution —. (page 143) [emphasis suppled]

WEiT’s perceptions of “Darwinism science” can be separated into two general categories:

(1) perceptions concerning process(s) of how major body plans (body forms) developed; and

(2) perceptions of the observed morphological character of extinct and extant body plans.

Concerning these two categories, the following observations are in order.

First Category.

The book’s discussions involving the first category (how major body forms diversified) are characterized by terminology that, beyond reasonable argument, represent speculation.

As an example of WEiT’s apparent disregard for avoiding “speculation,” the reader is encouraged to closely review WEiT’s presentation of perhaps the most famous of all transitional forms: the crow-sizes Archaeopteryx lithographica,” and note the use of speculative terms” such as (from page 40 thru 47) probably, suggest, could have been, unlikely, we don’t know, guesses, might have, and could also have which are offered as evidence for the processes and mechanisms of natural selection that relate to the diversification of major forms (major body plans). [underlining substituted for original italicized text]

Concerning the appearance of traits that presumably contributed to the move of animals from land to water, one of our best examples of an evolutionary transition:

Thanks to an amazing series of fossil finds in the Middle east, we can trace the evolution of each of these traits — from a terrestrial to an aquatic form. — There is no need to describe this transition in detail, as the drawings clearly speak — if not shout — of how a land-living animal took to the water. — The sequence begins with — a raccoon-sized animal called Indohyus. Living 48 million years ago, Indohyus was, as predicted, an artiodactyl. (page 49) [underlining substituted for original italicized text-other emphasis supplied]

But as in the speculative description of Archaeopteryx development, the discussion of how this series of body plans developed, there occurs the following terms that are anything but scientific: probably, almost certainly (a curious terminology-almost plausible?), what might well be, must have, and could not have.

Second Category.

But discussions involving the second category represent WEiT’s major efforts to establish support for why “it” is true and these take the form of predictions that WEiT, in one form or another involves transitional implications, which are claimed as proofs that establish the scientific “truth” of Darwinism.

This observation is grounded in WEiT’s own observation:

So how do we test evolutionary theory against the still popular alternative view that life was created and remained unchanged thereafter? There are actually two kinds of evidence. The first comes from using the six tenents of Darwinism to make testable predictions. By predictions, I don’t mean that Darwinism can predict how things will evolve in the future. Rather, it predicts what we should find in living or ancient species when we study them. (page 17) [underlining substituted for original italicized text-other emphasis supplied]

The record in the rocks confirms several predictions of evolutionary theory: gradual change within lineages, splitting of lineages, and the existence of transitional forms between very different kinds of organisms. (page 53) [emphasis supplied]

But other WEiT perceptions shed a different interpretation on the plausibility of the foregoing perceptions, particularly in reference to observed evidence involving the development of morphological diverse forms (body plans) which is the central product of the Darwinism hypothesis and thus relates to the central concept of predictions and scientifically based observations:

To really see the power of selection, we must extrapolate the small changes that selection creates in our lifetime over the millions of years that it has really had to work in nature. (page 143) [emphasis supplied]

We’ll never be able to reconstruct how selection created everything — evolution happened before we were on the scene, and some things will always be unknown. (page 137) [emphasis supplied]

We are at somewhat of a handicap here because, as we know, complex features take a long time to evolve, and most of them did so in the distant past when we weren’t around to see how it happened. (page 136) [emphasis supplied]

— the onus is not on evolutionary biologists to sketch out a precise step-by-step scenario documenting exactly how a complex character evolved. That would require knowing everything about what happened when we were not around — an impossibility for most traits and for nearly all biochemical pathways. (page 138) [emphasis supplied]

And it is particularly critically to reemphasize from a foregoing quote:

By predictions, I don’t mean that Darwinism can predict how things will evolve in the
future.

WEiT follows the foregoing analytical thrust with examples of what it perceives to constitute evolutionary predictions (paraphrased herein for brevity and emphasis):

— evidence for evolutionary change in the fossil record;

— cases on speciation in the fossil record — one line of descent dividing into two or more;

— new species forming in the wild;

— species that link major groups suspected to have common ancestors;

— species show genetic variation for many traits;

— should be able to find cases of imperfect adaptation;

and last but first;

— should be able to see natural selection acting in the wild.

Closely following these example of evolutionary-prediction categories, WEiT closes the chapter with the following:

As we’ll see, all the evidence — both old and new — leads ineluctably to the conclusion that evolution is true. (page 19) [emphasis supplied]

It is beyond the necessity of this post’s arguments to treat the myriad of predictions that WEiT presents that fall into one or more of the foregoing categories and thus the evaluation concentrates on the book’s dependence on transitional forms as evidence of evolutionary predictions that have been fulfilled.

By its own admission, the following is a typical representation of the book’s perspective of transitional forms as prediction:

One of the greatest fulfilled predictions of evolutionary biology is the discovery, in 2004, of a transitional form between fish and amphibians. This is the fossil species Tiktaalik roseae, which tells us a lot about how vertebrates came to live on the land. Its discovery is a stunning vindication of the theory of evolution. (page 35) [underlining substituted for original italicized text-other emphasis supplied]

In connection with the foregoing treatment of speculation in reference to Archaeopteryx lithographica:

Archaeopteryx lithographica, has just the combination of traits one would expect to find in a transitional form. (page 40) [underlining substituted for original italicized text-other emphasis supplied]

WEiT leaves no doubt that transitional-form discoverys represent fulfilled Darwinism predictions:

But we can make another testable evolutionary prediction: someday we’ll find fossils of feathered dinosaurs that are older than Archaeopteryx. (page 44) [underlining substituted for original italicized text-other emphasis supplied]

While we may speculate about the details, the existence of transitional fossils — and the evolution of birds from reptiles — is fact. — Scientists predicted that birds evolved from theropod dinosaurs, and, sure enough, we find theropod dinosaurs with feathers. (page 47) [emphasis supplied]

And revisiting the treatment of Indohyus above:

The sequence begins with — a raccoon-sized animal called Indohyus. Living 48 million years ago, Indohyus was, as predicted, an artiodactyl. (page 49) [underlining substituted for original italicized text-other emphasis supplied]

And last but not least as per WEiT’s evaluation:

And of course there is the human fossil record, described in chapter 8 — surely the best example of an evolutionary prediction fulfilled. (page 52) [emphasis supplied]

This “the best” whereas whale evolution was only one of the best.

Furthermore, WEiT states:

Obviously, we can’t replay the evolution of whales to see the reproductive advantage of each small step that took them back to the water. (page 125) [emphasis supplied]

Other than the examples treated herein, WEiT offers numerous additional prediction events, that in one way or another, involve transitional states of presumed morphological development sequences, to wit:

The theory of NATURAL SELECTION predicts what types of adaptations we’d expect to find —. (page 125) [emphasis supplied]

Everything we require of evolution by natural selection was amply documented by the Grants in other studies: individuals in the original population varied in beak depth, a large proportion of that variation was genetic, and individuals with different beaks left different numbers of offspring in the predicted direction. (page 134) [underlining substituted for original italicized text-other emphasis supplied]

Scott Carrol and his colleagues predicted that this host switch would cause natural selection for changes in beak size. (page 135) [emphasis supplied]

The fundamental problem in WEiT’s use of transitional information in a predictive sense is illustrated in the book’s discussion of blood clotting proteins, again paraphrased herein for brevity and emphasis:

— blood-clotting in vertebrates is a complicated reaction sixteen steps long;

— altogether more than twenty proteins are involved;

— evidence indicates the system could have been built up in an adaptive way from simpler precursors;

—once they arise, such duplicated genes can then evolve along separate pathways;

— we know that other proteins in the pathway had different functions in groups that evolved before vertebrates;

— fibrinogen is a blood-clotting protein that occurs in all vertebrates with a presumed different function in the vertebrates ancestral invertebrates;

— there must have been an ancestral protein from which fibrinogen evolved;

— Russell Doolittle predicted that such a protein would be found;

— and it was discovered in the sea cucumber.

WEiT summarizes the foregoing with:

This means that the common ancestor of the sea cumber and vertebrates had a gene that was later co-opted in vertebrates for a new function, precisely as evolution predicts. (page 140) [emphasis supplied]

In summary of WEiT’s perspectives presented herein:

Once sufficient information has been observed to indicate that a feature is a part of a development sequence, it is predicted that other stages of the development sequence had occurred and when a new feature in the sequence stage is observed, evolutionary biology has achieved another scientifically-derived evidence example of its predictive power.

The crux of WEiT’s logic on scientific evidence (to be treated in the next post) relates to the question in the forgoing summary that concerns a pattern that runs throughout the book’s perceptions of evidence that supports Darwinism:

WEiT perceives that newly observed (discovered) features (whether major morphological forms or traits associated with such forms) in previously observed organismal sequences, whose observations lead to the anticipation of new features in the sequence, i.e., formulation of the predictions, are fulfilled predictions that prove Darwinism is true.

Did WEiT, knowingly or unknowingly, commit a cardinal scientific error in the nature of a “syllogistic faux-naif?”

If so, then a clear conclusion can be drawn concerning the scientific quality of WEiT’s proofs of Darwinism.

POST 33: Natural Selection-WEiT's Missing Components

2011-01-02T19:13:00.000-08:00

On page 3, after the following the statement:

Life on earth evolved gradually beginning with one primitive species --- perhaps a self-replicating molecule --- that lived more than 3.5 billion years ago; it then branched out over time, throwing off many new and diverse species; and the mechanism for most (but not all) of evolutionary change is natural selection. [emphasis supplied]

WEiT writes:

When you break that statement down, you find that it really consists of six compoments: evolution, gradualism, speciation, common ancestry, natural selection, and nonselective mechanisms of evolutionary change. [emphasis supplied]

This post argues that WEiT's list of "components" does not include the following six "components" that are organismal and environmental conditions on which and in which the presumed mechanism of natural selection operates

It is thus appropriate to examine the presumed natural selection mechanism in terms of what these “components” contribute to the description of the presumed natural selection mechanism of processes.

1. Transitional forms are central to the concept of natural selection.

2. Major forms are the developmental condition of transitional forms.

3. Traits are features that change in the process of developing new major forms.

4. Geologic time is required for traits to develop into major forms.

5. Organism complexity is developed over extensive geologic time.

5. Environmental conditions are the “agents” that produce organism complexity.

6. Processes of mechanisms are the “operational controls” of environmental conditions.

To avoid the appearance of citing materials that misrepresent WEiT’s perspective and to establish beyond argument the key points of natural selection, extensive quotes are referenced for each of the major features on which this post bases its conclusions.

Likewise, the weight of this post’s arguments that challenge WEiT’s perceptions rest on the book’s fundamental beliefs that require a representative sample of quotes to establish the book’s basic ideology that significantly effects the interpretation of the single factor flavor of WEiT’s treatments.

Previous treatments of WEiT's and alternative perspectives of the natural selection in different contexts than in this post were presensed in Posts 19, 20, 21 and 22.

TRANSITIONAL FORMS

What really excites people — biologists and paleontologists among them — are transitional forms: those fossils that span the gap between two very different kinds of living organisms. (Page 32) [underlining substituted for original italicized text-other emphasis supplied]

— we have lots of evidence for common ancestors and transitional forms —. (page 26) [emphasis supplied]

A “transitional species” is not equivalent to “an ancestral species”; it is simply a species showing a mixture of traits from organisms that lived before and after it. (Page 35) [emphasis supplied]

ASSESSMENT

Earlier treatments of transitional species and major morphological forms (posts 14, 15, 16 and 17) cover assessments that are pertinent as overviews of the concepts as perceived by WEiT.

The book’s Chapter 2 entitled “Written in the Rocks” contains examples and discussions that are representative of the WEiT’s general approach for establishing why natural selection contributes to “Why” it is true , and is supported with comparable discussion formats in a section entitled “Selection in the Wild” in chapter 5 (The Engine of Evolution).

In both of these chapters, the principal source of information upon which WEiT bases its presentations on “transitional forms” as interpreted from fossil records.

The dominant feature in WEiT’s evidence for natural selection is the occurrence of transitional forms — information based on “transitional forms” constitutes a central theme (Chapter 2-Written in the Rocks) of the book’s defense of natural selection as the primary mechanism responsible for observed morphological diversity, i.e., major morphological changes, i.e., major body-plan changes.

It is pertinent to point out a subtle error in logic that applies to all of WEiT’s use of “transitional forms” in relation to natural selection — transitional forms may well represent a form between a before form and an after form but in reality a transition form is an after form in relation to its presumed predecessor and a before form in relation to its presumed descendant. (see Post 32 for an indepth perspective of "before" and "after" in relation to transitional forms)

But since “transitional forms” display morphological traits exhibited by a “precursor” organism and its presumed “descendant” organism, such forms constitute morphological conditions that occurred before and after a change process associated with natural selection and do not serve as evidence of the natural selection’s processes and mechanisms.

It would be excessively space consuming to bring under examination the individual transitional organisms that WEiT presents as supporting evidence based on observations in the fossil record, thus selected examples are addressed herein that establish the book’s general perceptions.

Concerning the presumed development of birds from dinosaurs:

A reading of WEiT’s explanations of the reptile to bird development (starting on page 39) is a critical example of “speculative” associations that are typical in the book.

All the nonflying feathered dinosaur fossils date between 135 and 110 million years ago. (Page 44)

Concerning whale development from land animals:

An example of “speculative” reasoning in terms of the processes of natural selection’s role in the book’s illustrations of land to water “adaptations," beginning on page 48.

This is one of our best examples of an evolutionary transition, — showing their movement from land to water. — transition, spanning the period between 51 and 40 million years ago. (Page 49)

Concerning natural selection in relationship to the hairy mammoth:

a bit hairier and let this process continue over some thousands of generations: (page 11)

Concerning trilobite ribs:

fossils from a layer of Welsh shale spanning about three million years — showed evolutionary change in the number of pygidial ribs. — and as stated above — we have no idea what selective pressures drove the evolutionary changes in these plankton and trilobites. (Page 31)

In effect all of WEiT’s “transitional form” examples, regardless of the context of the subject at hand, represent organisms whose morphological trait characteristics have completed, for their morphological stage, a change process and are thus “post natural selection” organisms.

Thus, transitional forms, whether discussed by example or by detailed rhetoric, do not provide evidence to support the concept of natural selection as perceived by WEiT and the generalized evolutionary biology field, i.e., as the “body plan fixation” mechanism in the development of major morphological features, i.e., major body plans.

In short, “transitional forms” are only a new completed body form that presumably represents an “in between form” and as such do not represent a transition process.

MAJOR FORMS

— because the fossil record is incomplete, we can’t expect to document every transition between major forms of life. (Page 25) [underlining substituted for original italicized text-other emphasis supplied]

And we have transitional fossils connecting many major groups. (Page 29) [emphasis supplied]

When writing the origin , Darwin bemoaned the sketchy fossil record. At the time we lacked transitional series of fossils or “missing links” between major forms that could document evolutionary change. (Page 26) [underlining substituted for the original italicized text-other emphasis supplied]

ASSESSMENT

WEiT’s perspective of transitional forms is essentially based on major forms, i.e. major body plans primarily treated in terms of fossils in Chapter 2 (Written in the Rocks).

Major forms are characterized as major body plans that have undergone sufficient trait changes to be recognized as something different from any preceding body plan, i.e. preceding “major form.”

The central role of major forms in the natural selection system is their identification with transitional forms.

This transitional form/major form relationship establishes a criterion that eliminates many of WEiT’s body-change examples that are based on morphological-structure duplications (or other minor alterations of continuous morphological structures (see Posts 5 and 6) from their use by WEiT observations that support the concept of natural selection.

Furthermore, major forms are to be interpreted as geologic-time phenomena, not human-experienced time spans that WEiT frequently addresses in terms of “what we may expect to see.”

TRAITS

Every species is pretty well adapted, which means that selection has already brought it into sync with its environment. Episodes of change that occur when a species meets a new environmental challenge are probably rare compared to periods when there’s nothing new to adapt to. (page 133) [emphasis supplied]

We may never have enough information to reconstruct the evolution of many traits, or even, in extinct species, to understand precisely how those traits functioned. (page 120) [emphasis supplied]

But it's hard to prove that a trait has absolutely no selective advantage. Even a tiny advantage, so small as to be unmeasurable or unobservable by biologists in real time, can lead to important evolutionary change over eons. (page 124) [emphasis supplied]

But if we can see selection causing small changes [small or unobservable trait?] over just a few generations, ---. (page 125) [bracketed text supplied]

--- complex features [complex traits?] take a long time to evolve, and most of them did in the distant past when we weren't around to see how it happened. (page 136) [bracketed text supplied-emphasis supplied]

That would require knowing everything about what happened when we were not around --- an impossibility for most traits and for nearly all biochemical pathways. (page 138) [emphasis supplied]

evolution: Genetic change in populations, often producing changes in observable traits or organisms over time. (page 248) [emphasis supplied]

ASSESSMENT

It is pertinent to establish that although WEiT uses the terms “trait” and “adaptation” repeatedly, it never defines the term trait beyond relating it to a wide variety of specific organismal features such as; rudimentary pelvis and hind legs (in the whale), eye color, blood type, height, weight, biochemistry (all from page 118), tetrapod limbs (from page 136), to gather, eat, digest (from page 134) and steps in the development of bird flight (gliding, flapping) which seems to imply that a “trait” is any morphological feature or function exhibited by an organism.

Concerning adaptations, WEiT essentially treats the concept as traits as implied in the following definition in the book's Glossary:

adaptation: A feature of an organism that evolved by natural selection because it performed a certain function better than its antecedants. (page 247)

At each stage of development, (conceptually parallel with WEiT’s perception that such development occurs in many small steps), the “trait” at that stage of development, as a component of body plan transitional forms, must be the result of a completed natural selection event, and as perceived by WEiT’s “nothing new to adapt to” in the traits quoted above.

The implication of this single WEiT quote in relation to the mechanisms of natural selection: the traits of the organism are in sync with environmental conditions which must imply that the organism’s traits are constantly in an adjustment process with the constantly changing environmental conditions (see ENVIRONMENTAL CONDITIONS section below).

In relation to the treatment of environmental conditions below, the observation by WEiT that traits are apparently in ”sync” with environmental conditions is critical.

As treated in Posts 11 and 12, the "other side of the coin," not treated in this post in its relationship to natural selection, is the equally important subject of trait origin.

GEOLOGIC TIME

— selection was extremely slow, altering populations over thousands or millions of years. (Page 116) [emphasis supplied]

—over many generations a species can evolve into something quite different: (page 3) [emphasis supplied]

It takes many generations to produce a substantial evolutionary change (such as the evolution of birds from reptiles). (page 4) [parentheses and other emphasis supplied]

— natural selection can, over eons, sculpt an animal or plant into something that looks designed. (page 11) [emphasis supplied]

— for most groups we see gradual evolution from earlier forms (birds and mammals, for example, evolved over millions of years from reptilian ancestors). (page 28) [emphasis supplied]

But when we’re talking about really big change, we’re usually referring to change that requires many thousands of years. (Page 4) [emphasis supplied]

To really see the power of selection, we must extrapolate the small changes that selection creates in our lifetime over the millions of years that it has really had to work in nature. (Page 143) [emphasis supplied]

We’ll never be able to reconstruct how selection created everything — evolution happened before we were on the scene, and some things will always be unknown. ([page 137) [emphasis supplied]

ASSESSMENT

The development of major forms, herein interpreted as the conversion of a prior major body-plan into a completely new body plan, occurs over large time spans.

The association of geologic time with the natural selection concept, thus limiting evidence to fossils, rules out WEiT’s explanations (or examples) based on “observable” time span as evidence supporting the concept, as argued in the foregoing assessment of major forms.

ORGANISM COMPLEXITY

—the onus is not on evolutionary biologists to sketch out a precise step-by-step scenario documenting exactly how a complex character evolved. That would require knowing everything about what happened when we were not around–an impossibility for most traits and for nearly all biochemical pathways. (Page 138) [emphasis supplied]

Understanding the evolution of complex biochemical features and pathways is not as easy, since they leave no trace in the fossil record. Their evolution must be reconstructed in more speculative ways, trying to see how such pathways could be cobbled together from simpler biochemical precursors. [Page 138] [emphasis supplied]

And since many traits can affect an individual’s adaptation to its environment (its “fitness”), natural selection can, over eons, sculpt an animal or plant into something that looks designed. (Page 11) [emphasis supplied]

Sure, selection can change the beaks of birds, or the flowering periods of plants, but can it build complexity. (Page 136) [underlining substituted for original italicized text-other emphasis supplied]

Natural selection must also work with the design of an organism as a whole, which is a compromise among different adaptations. (Page 12) [emphasis supplied]

WEiT emphasizes the foregoing perspective with the following:

First, natural selection can promote the evolution of complex, interconnected biochemical systems in which all the parts are codependent —. (page 129)

ASSESSMENT

In considering WEiT’s perspective that environmental conditions constitute the driving force for natural selection, two last two observations (listed above) are of singular importance.

Meaningful follow-up explanations, that should address their implications on natural selection’s status as a “proven Darwinian concept,” are missing among the myriad of WEiT’s oblique proofs of the concept’s plausibility.

The essential import imbedded in WEiT’s perceptions concerning organism complexity is that constantly changing multiple traits (i.e., WEiT’s small steps) are simultaneously subjected to the effects of constantly changing multiple environmental conditions (see first quote in “ENVIRONMENTAL CONDITIONS), typically in relation to major morphological form changes, over time spans that typically cover millions of years.

This perception aligns with the “Correlated Progression” concept proposed by T. S. Kemp and treated at length in Post 6, which is essentially encapsulated in the following quote from that post:

The pattern of acquisition of new traits or trait states from the ancestral to the descendant phenotype consists of small changes in one trait at a time, spread over the whole set of traits. They evolve analogously to a line of people walking forwards hand in hand: any one of them can be a single pace in front of or behind the next, but no more without breaking the line. Conversely, no single trait, structural or physiological, ever evolves by more than a small increment without being accompanied by evolutionary changes in many others. Therefore, no single trait can ever be seen in isolation as a privileged cause of the transition, and so, in principle, there can be no identifiable key innovations. [emphasis supplied]

Although organism complexity in this post is basically treated as a general concept in its relation to natural selection, the true nature of natural selection as a process in trait changes is illuminated when functionality is taken into consideration, such as treated in Post 8.

ENVIRONMENTAL CONDITIONS

Environments themselves change sporadically, and unevenly, so the strength of natural selection will wax and wane. (Page 31) [emphasis supplied]

Unfortunately, we have no idea what selective pressures drove the evolutionary changes in these plankton and trilobites. It is always easier to document evolution in the fossil record than to understand what caused it, for although fossils are preserved, their environments are not. (Page 32) [emphasis supplied]

We’ll never be able to reconstruct how selection created everything — evolution happened before we were on the scene —. (page 137) [emphasis supplied]

— complex features take a long time to evolve, and most of them did so in the distant past when we weren’t around to see how it happened. So how can we be sure that selection was involved. (Page 136) [underlining substituted for original italicized text-other emphasis supplied]

ASSESSMENT

As recognized by WEiT in the foregoing quotes, the book’s fundamental perception concerning natural selection is that environmental conditions were responsible for the “major morphological changes” exhibited by organisms in the fossil record.

Environmental conditions constantly change, whether on a large “global climate” scale over vast time spans representing millions of years, or smaller “local land mass” scales over hundreds of thousands of years.

Furthermore, because the environmental conditions that were in effect during the times that major forms were undergoing body-plan change, as WEiT noted, those environmental conditions cannot be described at levels of detail pertinent to the complexity of environmental agents that were acting on the complexity of traits involved in the major form changes.

As stated earlier, it is not necessary to analyze a broad spectrum of the book’s examples that are presented as support for the concept of natural selection (as understood by the book’s perception of the science’s understanding) --- the contents of three sections that treat major form developments supply sufficient material for this post’s conclusion that the environmental conditions associated with these transitional-form changes are nothing more than speculation. (Onto the land: From Fish to Amphibians (page 35); Into the Air: Origin of Birds (page 39); and Back to the Water (page 47))

Note in these three sections, when environmental causes are discussed in relation to morphological form results, many of the critical relationships discussions contain terms such as; guess, might, not hard to envision, probably (numerous), suggests, could have been (numerous), might have, almost certainly, believe, what might well be, must have been, could not have, etc.

In view of WEiT’s assertion that there is no place in science for speculation, these are speculative statements that negate the book’s use of these morphological forms as support the natural selection concept.

More critical for the science, since the actual “causative” environmental conditions are unknown and, under current levels of scientific capabilities cannot be known, explanations pertaining to such, regardless of other arguments, reduce the central concept of biological evolution, and Darwin’s hypothesis, to little more than speculation.

PROCESSES OF MECHANISMS

— the mechanism for most (but not all) of evolutionary change is natural selection. (Page 3) [emphasis supplied]

Natural selection remains the only process that can produce adaptations. [page 13]

— Selection is not a mechanism imposed on a population from outside. — it is a process—. (Page 117) [emphases supplied]

We need only show that such a development, involving processes and constituents not unlike those we already know and can agree upon, is feasible. (page 138) [emphasis supplied]

ASSESSMENT

Processes and mechanisms were treated extensively in Post 29 and thus this post’s treatment of these subjects is limited to the degree necessary to relate the two subjects to natural selection.

Natural selection consists of a collection of processes that comprise the processes and mechanisms that effects the simultaneous changes of a complex of codependent traits to arrive at individual adaptation in which all adaptations are in synchrony with a constantly changing set of environmental effects on the traits.

WEiT’s reference to selection being a mechanism not imposed from “outside” is particularly interesting in light of the book’s comments related to “environmental conditions: being unknown environmental conditions.

WEiT does not specify what is meant by “outside.”

It bears restating from Post 32 a critical observation from Dolph Schluter’s evaluation of the status of natural selection as a proven process:

The first is that in virtually all cases of selection in Endler’s survey, the actual cause of selection was unknown. Although differential survival or reproductive success may be associated with a particular heritable trait, we still have no idea of the mechanism of selection in most cases. Selection may actually be occurring on another unmeasured trait associated with the measured trait. Understanding the mechanism of selection is important so we can judge whether the selection is the result of factors in the local environment, or food supply, or whatever. [emphasis supplied]

In short, this post demonstrates that complex traits changing in codependent unison requires mechanisms that are controlled by complex environmental conditions that work in coordinated unison.

Explaining the “constituents” (WEiT’s terminology-page ??) and processes (Carrol’s “Operational Instructions For The Toolkit” (Posts 19, 20 and 21)) involved in the concept of natural selection via environmental conditions is the challenge faced but not answered by WEiT and evolutionary biology if it is considered that WEiT represents the state of the science.

Furthermore, it is implied (in ENVIRONMENTAL CONDITIONS and GEOLOGICAL TIME) by WEiT that the challenge, i.e., demonstrating the “codependant” change of a complex of traits that must proceed in synchrony with the complementary “cofunctional” environmental conditions), cannot be met (at least in terms of the current “scientific” technology).

The fundamental problem associated with the processes and mechanisms involves both environmental conditions and trait conditions.

As treated in Post 26, which process initiated the natural selection-biological trait interaction: did a trait change thus setting the stage for an appropriate change in environmental conditions to established the trait as an adaptation; or did an environmental condition develop setting the stage for an appropriate trait change to establish the trait as an adaptation; or did the environmental condition and the biological trait change at the same time, as depicted in Post 25?

Post 32: Natural Selection-WEiT's Misconceptions

2010-12-04T09:46:00.000-08:00

Representing something in the nature of a final declaration of the book’s perspective concerning the status of evolutionary biology’s concept of natural selection, WEiT offers the following:

There are many more examples, but they all demonstrate the same thing: we can directly witness natural selection leading to better adaptation. Natural Selection in the Wild, a book by the biologist John Endler, documents over 150 cases of observed evolution, and in roughly a third of these we have a good idea about how natural selection was acting. — How many more examples do we need? (page-136) [underling substituted for WEiT’s italics-other emphasis supplied]

The final sentence in the foregoing WEiT quote (“How many more examples do we need”) establishes the subject of this post —to establish with reasonable plausibility that WEiT should have asked the question —do any of the examples demonstrate plausible observations (beyond a “good idea”) of natural selection in operation, i.e. natural selection mechanisms and processes?

The critical feature for this post’s rationale rests in establishing the distinction between the concepts of natural selection and adaptation and more specifically the difference in evidence that has been documented through observations.

Although the biological evolution literature abounds with “definitions” of these two concepts (some of which differ significantly), it is appropriate to base this post’s perspectives on definitions from the source containing the proposed evidences of the two concepts —Endler’s paper.

The following quotes from Endler’s paper (83) serve to define natural selection:

When properly defined, natural selection is a syllogism rather than a tautology. Natural selection is a process which results from biological differences among individuals —. [emphasis supplied]

To reiterate: natural selection is a process resulting from the interactions between variable organisms and environment, — . [emphasis supplied]

The important and interesting questions in studies of natural selection are: (1) What are the biological reasons that confuses cause and effect, and focuses attention away from causes — ? [emphasis supplied]

Natural selection cannot “generate genetic changes within populations,” it is a process, resulting from heritable biological differences among individuals — . [emphasis supplied]

Natural selection is not an explanation for adaptation; it only explains why and how relatively better adaptations can increase in frequency. The answer to why a given adaptation is superior to an alternative one, or why condition b for natural selection occurs, is a question of the mechanism of origin of new variants, the history of their origin and spread, and biological and ecological reasons for conditions a - c for the variants, and the conditions themselves. — To say that a new adaptation necessarily arose through natural selection is an incomplete description, a tautology, and a misrepresentation of natural selection, adaptation, and evolution. Natural selection addresses the problem of the spread of new variants or new adaptations, not their origin. [underlining substituted for the original italicized text – other emphasis supplied]

Endler’s “definitions” of natural selection appears to be in line with and perhaps more directly stated in following:

From Wikipedia:

Natural selection is the process by which traits become more or less common in a population due to consistent effects upon the survival or reproduction of their bearers. It is a key mechanism of evolution. [emphasis supplied]

From Encyclopaedia Britannica:

Natural selection: process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype, or genetic constitution. [emphasis supplied]

From Stanford Encyclopedia Of Philosophy:

Natural selection is a causal process. [emphasis supplied]

For the purposes of this post’s arguments, the foregoing “definitions” of natural selection exhibit one critical feature concerning the nature of natural selection — it is a process, a mechanism comprising components that perform a function — it is not an observed result or consequence.

WEiT confirms this post’s foregoing perspective of natural selection as a process with the following:

Selection is not a mechanism imposed on a population from outside. Rather, it is a process, a description of how genes that produce better adaptation become more frequent over time. When biologists say that selection is acting “on” a trait, they’re merely using shorthand to say that the trait is undergoing the process. (Page 117) [bold emphasis supplied]

Three things are involved in creating an adaptation by natural selection. (Page 117) [emphasis supplied]

And quoting Olga Zhaxybayeva’s argument concerning flagellar evolution:

Evolutionists need not take on the impossible challenge of pinning down every detail of flagellar evolution. We need only show that such a development, involving processes and constituents not unlike those we already know and can agree upon, is feasible. (Page 138) [emphasis supplied]

By noting that natural selection is a “process” that is comprised of functional parts, i.e., the processes “constituents,” WEiT acknowledges that claimed observations, or other sources of description, must incorporate a description of the processes parts and an explanation of how the parts function as the mechanism that results in an adaptable “trait.”

Concerning the “definition” of adaptation, the following (85) clearly separate this concept from the concept of natural selection:

— adaptations are traits (or characters) that have been subjected to natural selection—. This means that the trait has "evolved" (been modified during its evolutionary history) in ways that have contributed to the FITNESS of the organism manifesting it . [emphasis supplied]

Reeve & Sherman (1993) speak of "adaptation" as a consequence" ". . . a phenotypic variant that results in the highest fitness among a specified set of variants in a given environment" This "definition” of adaptation consists of three components: (1) a set of phenotypes, (2) a measure of fitness, and (3) a clearly defined environmental context" (the current environmental situation, involving both biotic and abiotic elements.) [emphasis supplied]

An evaluation of Endler’s perspectives on how his studies demonstrated natural selection at work keys on what his observations actually represent— are they observations that pertain to natural selection or, are they observations that pertain to adaptation?

Since Elder’s book is widely acknowledged in learned biological evolution literature as premiere evidence on the status of natural selection’s role in biological development (and as implied by the nature of WEiT’s citation), an evaluation of Elder’s observations in a paper by Dolph Schluter (84) casts a somewhat different perspective on those observations than perceived by WEiT (and also provides the basis for further examination of other “examples” of natural selection offered by WEiT).

The first is that in virtually all cases of selection in Endler’s survey, the actual cause of selection was unknown. Although differential survival or reproductive success may be associated with a particular heritable trait, we still have no idea of the mechanism of selection in most cases. Selection may actually be occurring on another unmeasured trait associated with the measured trait. Understanding the mechanism of selection is important so we can judge whether the selection is the result of factors in the local environment, or food supply, or whatever. [emphasis supplied]

After discussing two additional problems with Endler’s results (important but not directly relevant to the emphasis of this post), Schluter adds the following:

It is therefore difficult to extrapolate from the measurement of apparent selection to the kind of selection that may be operating. [emphasis supplied]

In a section entitled “Criteria for Demonstrating Natural Selection,” Schluter treats subject matter that leads to the second argument posited in this post:

The first criterion that Endler used to include examples of selection in his survey was that the traits were heritable, or were thought to be heritable; that is, the traits had a genetic basis, at least in part. — A direct demonstration of selection is made by marking a sample of individuals and measuring them for a trait before and after selection, or by repeatedly measuring a trait in an unmarked cohort of individuals in a single age class. [underlining original-other emphasis supplied]

The critical feature of Schluter’s foregoing statement is the “before and after” conditions of Endler’s cited examples of documented natural selection.

Natural selection occurs between Endler’s “before” and “after” trait observations and thus was not observed or otherwise documented and therefore do not represent observations of natural selection

Since WEiT relies on numerous examples of claimed observed natural selection to buttress its perception of why evolution is true, the perception’s credibility rests significantly on whether its examples meet the definition(s) of natural selection as discussed herein, or whether they are actually “before” and “after” descriptions.

Examination of WEiT’s natural selection examples will be the subject of future posts.

Literature Cited:

83. Endler, J. A. Natural Selection in the Wild. Princeton University Press, Princeton, NJ. 1986.

84. Schluter, Dolph. Selection And Variability In Natural Populations. U. S. Dept. Commerce/NOAA/NMFS/NWFCS/Publications. NOAA Tech Memo NMFS NWFSC-30.

85. Deep Ethology: Evolution Adaptation: https://notes.utk.edu/.../6febf994e87a160e85256cff00668214?...

Post 31: Natural Selection-Misconceptions?

2010-11-16T15:37:00.000-08:00

Although literature concerning biological evolution involves educational motives, those motives are generally in company with a primary intent of contributing newfound knowledge or understanding.

WEiT makes it clear that its motive is to teach Darwinian concepts to those who lack a sufficiently understanding of the hypothesis, as per the following statement:

—But for many who find themselves uncertain, or who accept evolution but are not sure how to argue their case, this volume gives a succinct summary of why modern science recognizes evolution as true. I offer it in the hope that people everywhere may share my wonder at the sheer explanatory power of Darwinian evolution, and may face its implications without fear. (page xiv) [emphasis supplied]

This understanding rests largely with one Darwinian concept:

—it [evolution] happened largely as Darwin proposed, through the workings of natural selection. (page xiv) [bracketed text and emphasis supplied]

This simple and profoundly beautiful theory, the theory of evolution by natural selection, has been so often misunderstood, and even on occasion maliciously misstated, that it is worth pausing for a moment to set out its essential points and claims. (page 3) [emphasis supplied]

These foregoing quotes from WEiT frame the subject of this post: teaching natural selection to overcome its misunderstanding.

The foregoing WEiT perspectives lead to two questions:

What is conveyed in instructional publications that leads to misunderstanding?

And

What needs to be conveyed to prevent misunderstanding.

These two questions are specifically addressed in an article in the second volume of the 2009 issue of the magazine Evolution Education Outreach, entitled “Understanding Natural Selection: Essential Concepts and Common Misconceptions” by T. Ryan Gregory.

Since the magazine specifically targets the education of the teaching profession, and since there has been no follow ups with corrections, clarifications or other evaluations (as far as this blog can determine), concerning a myriad of misconceptions about misconceptions, the article is assumed herein to represent a “state-of-the-art” example of what the misconceptions are and how to correct them.

Gregory establishes the paper’s “objectives” (this post’s terminology) as follows:

This paper provides an overview of the basic process of natural selection, discusses the extent and possible causes of misunderstandings of the process, and presents a review of the most common misconceptions that must be corrected before a functional understanding of natural selection and adaptive evolution can be achieved. [emphasis supplied]

–this article is aimed at readers who wish to confront and correct any misconceptions that they may harbor and/or to better recognize those held by most students and other non-specialists. [emphasis supplied]

Understanding this process is therefore of considerable importance in both academic and pragmatic terms. Unfortunately, a growing list of studies indicates that natural selection is, in general, very poorly understood — not only by young students and members of the public but even among those who have had postsecondary instruction in biology. [emphasis supplied]

— natural selection is so logically compelling that its implications become self-evident once the basic principles have been conveyed. [emphasis supplied]

The goal of this paper is to enhance (or, as the case may be, confirm) reader’s basic understanding of natural selection. [emphasis supplied]

Gregory partitions his perspective of natural selection “misconceptions” into five sections and nineteen sub sections each of which breaks misconceptions into further levels of detail.

A subsection entitled “Conceptual Frameworks Versus Spontaneous Construction” contains a perspective of natural selection that in effect establishes the fundamental concepts upon which explanations must relate in order to accomplish “What needs to be conveyed to prevent misunderstanding.”

In addressing the problem of misconceptions, Gregory states:

Overall, the issue does not seem to be a lack of logic —, but a combination of incorrect underlying premises about mechanisms and deep-seated cognitive biases that influence interpretations. [emphasis supplied]

And in reference to the “earlier” development of naive understandings of how the world is structured, presumably also natural selection:

These tend to persist unless replaced with more accurate and equally functional information. [emphasis supplied]

Thus the question is: does Gregory accomplish this need of explaining “mechanisms” and “functional information” that satisfies the paper’s five objectives as specified above.

An individual in-depth critique of each of the nineteen subsections would require something on the order of a voluminous book most of which would only confirm the following critique of the paper’s final section entitled “A Catalogue of Common Misconceptions” comprising the following subsections.

Teleology and the “Function Compunction”

In addressing the misconception of teleology, that is a perception of directed outcome:

Obviously, this contrasts starkly with a two-step process involving undirected mutations followed by natural selection (see Fig 2 and Table 3). [emphasis supplied]

The critical feature of Gregory’s Table 3, as a summary of this subsection, which is in effect an “explanation” of the other 18 subsections, is its perspective of “correct” and “incorrect” interpretations but the “explanations” are only descriptions of what the concepts imply and do not imply — the explanations do not contain descriptions of how the actual “processes” and/or “mechanisms” work, in effect Gregory’s “functional information.”

Anthropomorphism and Intentionality

The subject matter is in effect largely parallel with the foregoing subsection — misconceptions associated with Gregory’s perception of “conscious intent.”

Nothing in terms of “processes”, “mechanisms” or “functional information” is addressed.

Use and Disuse

Addresses Lamarckian perception of trait origin and inheritance without relating the concept to actual “processes”, “mechanisms” or “functional information.”

Soft Inheritance

Essentially a re-statement of the foregoing subsection’s concept but supported by a flowchart illustrating a sequence of gene “conditions” or “occurrences” (“initially contains a gene” — “random mutation occurs” — “gene is passed” — “develops into”) that do not qualify as “processes”, “mechanisms” or “functional information.”

Nature as a Selecting Agent

Largely repetitive as a sort of summarization of foregoing subsections:

— natural selection cannot have plans, goals, or intentions, nor can it cause changes in response to need.

But the subsection does contribute a perspective that this post argues is a characteristic of Gregory’s presentations —the difference between a “description” (i.e., a "definition") and an “explanation:”

— students can recognize the distinction between an anthropomorphic or teleological formulation (i.e., merely a convenient description) versus an anthropomorphic/ teleological explanation (i.e., involving conscious intent or goal-oriented mechanism as causal factors: —. [bold emphasis supplied—underlining substituted for his italicized text]

Source Versus Sorting of Variation

Essentially a restatement of soft inheritance as presented above stressing that:

— natural selection itself does not create new variation. [—underlining substituted for his italicized text]

Typological, Essentialist, and Transformationist Thinking

Largely repetitive of previous subsections , but contains the following as an example of the problems typical in this paper:

The incorrect belief that species are uniform leads to “transformationist” views of adaptation in which an entire population transforms as a whole as it adapts ---. [emphasis supplied]

but

Organisms do not evolve; populations evolve. [—underlining substituted for his italicized text][from subsection “Natural Selection and Adaptive Evolution”]

and

By contrast, natural selection actually occurs continually and simultaneously within entire populations —. [emphasis supplied][from subsection “Events and Absolutes Versus Processes and Probabilities”]

— it must be noted that fitness refers to reproductive success relative to alternatives here and now — natural selection cannot increase the proportion of traits solely because they may someday become advantageous. Careful reflection on how natural selection actually works should make it clear why this is so. [bold emphasis supplied---underlining substituted for his italicized text]

These are some of the more conspicuous examples of what appears to represent off-handed comments to meet an immediate need rather than a logically crafted explanation.

Events and Absolutes Versus Processes and Probabilities

The following comment, in connection with the final quote in the foregoing subsection suffices to lead this post’s argument into the next phase:

Natural selection is mistakenly seen as an event rather than a process —. [bold emphasis supplied---underlining substituted for his italicized text]

An appropriate measure of Gregory’s misconception analysis if their contribution, as he stated in a foregoing quote, understanding this process (of how natural selection works).

One sentence in his paper provides a central concept whose information requirements are integral for any explanation to aid understanding the process and can be viewed as the holy grail of essentials for such understanding.

Natural selection results from the confluence of a small number of basic conditions of ecology and heredity. [emphasis supplied]

From Gregory’s (and WEiT’s) perception of the need to clearly articulate the concept of natural selection, the key features of the foregoing statement lie in the relationship between “confluence” and “basic conditions” to which must be added how natural selection actually works .

Specifically, what are the elements of an ecological condition that establish the “confluence” relationship with the “heredity” traits and what are the elements of “heredity” traits that the specific “ecological elements” act on?

The contribution to the paper’s stated goal of advancing the understanding of how natural selection works lies in two observations in the paper, both of which relate to the concept of confluence.

The first involves the time element in the fixation of a new trait, i.e., the time period and length of time in which the confluence conditions exist.

The third section, entitled “Natural Selection and Adaptive Evolution” contains the following:

The important points are that this uneven reproductive success among individuals represents a process that occurs in each generation and that its effects are cumulative over the span of many generations. Over time, beneficial traits will become increasingly prevalent in descendant populations —. [emphasis supplied]

As the name implies, this is the process [adaptation] by which populations of organisms evolve in such a way as to become better suited to their environments as advantageous traits become predominant. On a broader scale, it is also how physical, physiological, and behavioral features that contribute to survival and reproduction (“adaptations”) arise over evolutionary time. [bracketed text and bold emphasis supplied]

The second section entitled “Darwinian Fitness” with a subsection entitled “Which Traits Are the Most Fit” contains the following which will be referenced below as the “Directional” quote:

Directional natural selection can be understood as a process by which fitter traits (or genes) increase in proportion within populations over the course of many generations. It must be understood that the relative fitness of different traits depends on the current environment. [A] Thus, traits that are fit now may become unfit later if the environment changes. [B] Conversely, traits that have now become fit may have been present long before the current environment arose, without having conferred any advantage under previous conditions. —fitness refers to reproductive success relative to alternatives here and now — natural selection cannot increase the proportion of traits solely because they may someday become advantageous. Careful reflection on how natural selection actually works should make it clear why this is so. [bold emphasis supplied][letters in brackets supplied for referencing below]

The foregoing of the paper’s perspectives lead to three fundamental questions:

1. Does the paper address the concepts of “time elements required for trait fixation?”

2. Does the paper address “confluence conditions?

3. Does the paper address the ecological elements and the hereditary trait elements.

Thus, the first basic problem faced by Gregory in documenting the process(s) that control natural selection and adaption lies in the relationship between the organism’s “traits-possible-for selection” and the environment’s “conditions available for selection” — specifically can evolutionary biology demonstrate “environmental conditions stasis” of sufficient duration for trait fixation to occur?

The second basic problems involves documenting specific features of a trait and specific features of the environment (or ecology) that are in “confluence?”

Thus, the critical aspect in the foregoing statement is that the fixation of an “advantageous trait” involves some period of time.

In a section of the caption related to Fig. 2 in Gregory’s paper, there occurs the following in reference to the first phase of the “correct” depiction of the sequence of natural selection:

(A) A population of organisms exhibits variation in a particular trait that is relevant to survival in a given environment. In this diagram, darker coloration happens to be beneficial, but in another environment, the opposite could be true. [emphasis supplied]

This by definition requires a period of time in which the “given environment” and the “advantageous trait” remain in sufficiently stable relationship for the “adaptation” to occur.

This perspective was addressed in Post 26 and the relevant aspects are re-treated here.

1. The adaptation conditions, the “confluence period,” must remain in effect for some time period of sufficient length for the consequence to be achieved.

2. The environmental elements associated with the “confluence conditions” must not deviate from the favorable “confluence conditions.”

The plausibility of this concept of adaptations place in natural selection rests on whether the environmental elements associated with the confluence conditions remain static or whether the environmental conditions continually changed during a time period required for fixation of a trait.

Two symbolic flowcharts are illustrated below that are centered on WEiT’s concepts of “well adapted” and “not so well adapted” organisms.

In Scenario 1 below, equivalent to statement [A] in the above “directional natural selection quote, the natural selection sequence begins with “trait” and “environment” coordinated to facilitate “adaptation” but the “environment” progress through a period of changes that do not facilitate a compatible fit of the “trait” with the “environment.”

In Scenario 2 below, equivalent to statement [B] in the above “directional natural selection quote, a “trait” has developed in an environment unfavorable for its “adaptation” but progresses through a period of environmental “condition” changes becoming “more favorable” and terminate in its “adaptation.”

If the “heredity/environment confluence” is altered by changing environmental conditions, as depicted in the foregoing scenarios, then there are grounds to argue that the whole concept of an adaptation existing in a “stasis” condition of sufficient time span to allow a population of organisms to attain a “well adapted” trait, (i.e., from an individual in which the trait originated, to a local population, to a larger geographic area population, as Eldredge states below), is not in fact the actual situation.

The essential question is the required “confluence-time stasis” that necessitates an environmental stasis, which does not appear to be the case as perceived by the following, all from source (82), which interestingly, is senior authored by the editor of the publication which contains Gregory’s paper.

Species-wide depletion of accessible beneficial mutations requires a degree of environmental constancy that is not typical of the earths history.(Lambeck and Chappell 2001; Zachos et al. 2001.) [emphasis supplied]

More recently, the geographic mosaic of ongoing local adaptation has become the very foundation for new views of how coevolving interactions between species persist over long periods of time in a constantly changing world (Thompson 1994, 1999a,b). [emphasis supplied]

The more variable the environment over time, the more restricted the range of these genotypes with equal or higher fitness, because each genotype must function under a wide range of environmental conditions. [emphasis supplied]

An environmental change, by redefining the “optimum” phenotype, may result in increasing the probability of mutations being conditionally advantageous or neutral, thereby promoting evolutionary change. [emphasis supplied]

A novel genotype must originate, become established in a local population, and then spread and increase in numbers across a large geographic area. [emphasis supplied]

The breakdown of stasis occurs as a local population adapts rapidly to an initially inhospitable habitat before it would otherwise be driven extinct. [emphasis supplied]

But more generally, the field of evolutionary ecology has clearly shown the ability of local populations to evolve rapidly under changing conditions. [emphasis supplied]

These foregoing perspectives by Eldredge et al. elevate the time span aspect of the environment and ecological stasis to a critical position in Gregory’s “confluence conditions” and create serious plausibility problems for the conventional perspective of “traits” becoming adapted solely by stasis of environmental/ecological conditions.

And last but not in any way the “least,” concerning the paper’s failure to heighten the understanding of how natural selection works is the absence of functional specifics.

It is logical in a learned course of inquiry to expect an explanation of the “functional relationships , i.e., the processes that Gregory repeatedly calls into play, between the specific environmental entities that interact with specific hereditary entities during the period of “confluence” relationships.

Perhaps the most plausible statement in the paper is Gregory’s perception that:

Teachers notwithstanding, “it appears that a majority on both sides of the evolution-creation debate do not understand the process of natural selection or its role in evolution” (Bishop and Anderson 1990).

This post concludes with the observation that Gregory’s paper falls into that majority.

Literature Cited:

81. Gregory, T. Ryan. Understanding Natural Selection: Essential Concepts and Common Misconcepts. Evo Edu Outreach (2009) 2: 156-175.

82. Niles Eldredge, John N. Thompson, Paul M. Brakefield, Sergey Gavrilets, David Jablonski, Jeremy B. C. Jackson, Richard E. Lenski, Bruce S. Lieberman, Mark A. McPeek, and William Miller III. The Dynamics of Evolutionary Stasis. Paleobiology 31(2). 2005.]

Post 30: WEiT's (And Evolution's) Russian Doll Problem-Molecular Aspect

2010-10-04T19:30:00.000-07:00

In anticipation of an "eyes rolled back in the head" reaction concerning the illustrations in this post, two preface statements of intention are in order.

First:
The series of flowcharts and biochemical/molecular structure illustrations ARE NOT intended as a treatment of how biochemical interactions and/or molecular structure changes relate to the phototransduction (vision process) cascade.

Second:
The illustrations ARE to demonstrate the extent that biochemical reactions and molecular structures, from the initiation to the termination of the phototransduction cascade (the sequence from reception of a light photon to electrical signal ready for transmission to the brain), are resorted to as explanations of "how phototransduction works."

In particular, the molecular structures are intended to demonstrate the "form of the forest" used in explanation rather than the "ecology of the particular trees" --- thus, for the purposes of this post, pay no attention to the phototransduction details --- it is the molecular structure dependence for explanation that is the relevant feature of the illustrations.

This post has as its goal the consideration of two biological evolution concepts, the “Russian Doll Model” as perceived by Gehring (67) and “The Dark Matter of the Genome” as perceived by Carrol (33), the likely relationship between the two concepts, and their implication on direction of evolutionary biology’s research direction toward documenting the processes mechanisms that guide the development of morphological diversity.

The focal point of the "Russian Doll Model" and "The Dark Matter Of The Genome" involves WEiT's following statement in reference to the molecular properties necessary to explain "Why Evolution Is True:"

The theory of natural selection has a big job–the biggest in biology. Its task is to explain how every adaptation evolved, step by step, from traits that preceded it. This includes not just body form and color, but the molecular features that underlie everything. (Page119) [emphasis supplied]

Gehring formulates his "Russian Doll Model" concept as follows:

This symbiont hypothesis, which I call the Russian doll model, assumes that light sensitivity first arose in cyanobacteria, the earliest known fossils on earth. These cyanobacteria were subsequently taken up by eukaryotic red algae as primary chloroplasts surrounded by an outer and inner bacterial membrane separated by a proteoglycan layer. Subsequently, the red algae were taken up by dinoflagellates as secondary chloroplasts surrounded by an additional third membrane coming from the primary red algal host. — Because dinoflagellates (also called zooxanthellae) are commonly found as symbionts in cnidarians, dinoflagellates may have transferred their photoreceptor genes to cnidarians. This is the most speculative step in the Russian doll model. [emphasis supplied]

Thus, in Gehring’s perspective, the first “doll’ to be opened is the “cinodarian doll,” which on opening reveals the “dinoflagellate doll,” which on opening reveals the “eukaryotic red algae doll,” which on opening reveals the “cyanobacteria doll.”

The essential characteristic of the Russian Doll concept rests in each newly revealed doll exhibits the same type of structure as the previous doll from which it emerged.

The argument in this post is to establish the parallel between the "Russian Doll Model" and what can be termed the "Molecular Phototransduction Model" in terms of new molecular descriptions and the implications for ultimately revealing Carroll's "Operational Instructions."

Burns et al. (68) summarizes the constant progression in biochemistry of molecular composition that evolutionary biology research has taken (restructured to emphasize sequence):

The biochemical and electrophysiological bases of phototransduction have been intensively investigated for decades.

● Early studies in this field led to the discovery of the first G protein-coupled receptor (GPCR), rhodopsin — .

● A century later, the solution of rhodopsin’s crystal structure, the only so far for any GPCR, has greatly expanded our understanding of the molecular mechanisms underlying GPCR signaling — .

● Functional studies of rhodopsin have resulted in the discovery of its light-dependent phosphorylation —

● and the first arrestin protein — .

● Eventually these studies led to the formulation of a general principle for GPCR inactivation in which full loss of its catalytic activity requires phosphorylation followed by arrestin binding — .

● The analysis of visual signaling downstream of rhodopsin has also yielded many fundamental findings.

● Studies of the phototransduction cascade have been instrumental in the elucidation of the function — and structure of G proteins —

● the development of a complete theory of signal amplification in GPCR cascades —

● the understanding that the duration of heterotrimeric G protein signaling can be regulated by acceleration of G protein GTPase activity —

● and the identification of the first cyclic nucleotide-gated channel —.

Following this developmental history, Burns' comment on new directions of research.

Recent years have also been marked by renewed interest in the electrophysiological processes in photoreceptor inner segments and synaptic terminals that ultimately filter and transmit the visual signal to second-order neurons. Finally photoreceptors are increasingly used as a model system for studying many cell biological questions, including cell polarity, protein sorting and intracellular trafficking, the assembly and targeting of multiprotein signaling complexes, and the mechanisms connecting the signaling events in the outer segments with cellular health and disease. [emphasis supplied]

The argument herein narrows from Burn's general perspective to the phototransduction concepts of the eye as representing biological evolution's "understanding" of mechanisms and processes, as expressed by Kandel (69) :

The retina bears careful examination for several reasons. First, it is useful for understanding sensory transduction in general because photoreceptors in the retina are perhaps the best understood of all sensory cells. Second, unlike other sensory structures, such as the cochlea or somatic receptors in the skin, the retina is not a peripheral organ but part of the central nervous system and its synaptic organization is similar to that of other central neural structures. [emphasis supplied]

In his introductory comments, Kandel sets a simple tone for launching a technically tedious discussion with the following:

This chapter is divided into two parts. In the first part we describe how phototreceptors transduce light [photons] into an electrical signal [to the brain]. In the second we consider how these signals are shaped by other retinal neurons before being sent to the brain. [bracketed text and emphasis supplied]

Thus, the series of biochemical/molecular illustrations below are symbolic of "modes of explanation" used, for the past several decades, to explain phototransduction research results .

As stated in this post's opening remarks, the foregoing illustrations are not intended as a review of "how" phototransduction "works," but are intended to provide a general picture of the mode that is used to explain the cascade.

Illustration 1 was adapted from Sturm (70) and illustrates the phototransduction cascade from reception of a light photon to electrical signal generation to the brain and the return of the eye biochemistry to receive a new photon.

Illustration 2 was adapted from a paper entitled "the Rhodopsin Cycle" (71) and essentially follows the cascade (in illustration 1) but in somewhat easier interpretation with additional detail.

Illustrations 3 and 4 were adapted from Isayama et al.. (72) and display more detailed biochemical properties of part of the phototransduction cascade.

Illustration 5 was adapted from Wikipedia (73) and illustrates the molecular structure of a biochemical in Illustration 4.

Illustration 6 was adapted from Casiday et al. (74) and illustrates the molecular structure of a biochemical in Illustration 4.

Illustration 7 was adapted from McBee et al. (75) and in part illustrates the molecular structures of a portion of Illustration 2 ("resetting" the cascade to receive a new photon).

Illustration 8 was adapted from Kuska et al. (76) and illustrates additional molecular detail from a section of Illustration 7.

Phototransduction research has proceeded on two general fronts: the quest for increased understanding of more detailed biochemical functions and molecular structures involved in phototransduction.

The results of this research lead to two basic "pictures" of the cascade as displayed in the foregoing illustrations both of which can be stated with reasonable certainty and are basic for the arguments treated below:

First:
For any given organism, the sequence of the cascade and associated biochemical reactions are fixed in a normal cascade execution --- the basic sequence of the cascade does not change.

Second:
For any given stage in a normal cascade execution, the points of alteration of molecules at that stage is fixed --- the points of alteration do not change.

This quest into increasing detail of biochemical interactions and molecular structure represents this post's perspective of Gehring's "Russian Doll Model" --- the sequence of molecular structures in essence represent a series of Russian Dolls each of which displays the previous "model's" general structural pattern of molecular organization.

This sequence of molecular Russian Dolls leads to the following question:

Is the acquisition of more detailed sequence of biochemical interactions and molecular structures, as represented in the phototransduction cascade, progressing toward a plausible explanation of the controlling mechanisms(s) (operational controls) that execute the biochemical and molecular cascade?

This question has an arguable basis in connection with the second major research thrust in phototransduction research --- the biochemical processes associated with the molecule-to-molecule alterations during the execution of the cascade.

Two major observations derive from research on biochemical effects:

First:
The process descriptions of the "natural" biochemical reactions that link the effects between sequential molecules;

Second:
The artificial modification of the between-molecule processes to diagnose or otherwise modify the processes for various medical objectives.

This post argues that the implementation of artificial modification of the natural biochemical relationships that modify the molecular structures, thereby modifying the nature of their effect on the impacted molecules, constitutes the undiagnosed presence of an "operational control" mechanism (to cite Carrol's perception of evolutionary biology's "dark matter").

Medical science's ventures toward artificially changing the effects of the biochemical process, and thus the structure of the involved molecules, in essence represents efforts to modify the "operational control" of the phototransduction cascade.

If this is a plausible deduction, then it follows that increased or additional detailed understanding of molecular structures, and identification of previously unobserved molecules in the phototransduction cascade, will not reveal the nature of the "operational controls."

This perception does not demean, for this post's objectives, the value of such additional molecular and/or biochemical knowledge, particularly to the medical sciences.

The foregoing perspective is given logical support in the application of mathematically specified computer simulations designed to mimic various effects involved in the phototransduction cascade.

The mathematical equations that execute these artificial phototransduction cascades, or small sequences therein, are in essence science's substitutes for their actual counter-part biological "operational controls."

Thus, the fundamental question toward which this post has been pursuing:

What is the biological nature of the "natural operational controls" represented by the mathematical equations?

Pattee (81) perceives the utility of these models as follows:

--- but at present there exists an enoromous gap between these statistical physics and artificial computer-life models and the complex, coded, semiotic control of life as we know it.

--- the weakness of this approach is that there is no attempt to address how descriptions control actual physical construction, and how constructions relate to function.

It is questionable, basis on the following treatments of "self-oganization" concepts, whether the current research direction toward increasingly detailed understanding of the biochemical processes and molecular structures will provide the answer.

Medical science proceeds in part in its research accomplishments by identifying malfunctions in the biochemical processes which occur at specific sites in effected molecules thus causing specific human health disorders, with the objective of artifically "correcting" the specific molecular structures that have become altered from their normal state

This perspective leads to a critique, at a fundamental level concerning the plausibility of evolutionary biology's basic concept of randomness in biological evolution (as in WEiT's perspective of small biological changes occurring as a result of random processes).

There is beyond argument a pattern of constancy, specifically an "operational control" constancy, that maintains a sufficient fixed state of control of the biochemical processes to provide an "expected stable operational state" to justify science's mathemically constructed simulations to mimic the phototransduction cascade.

The expectation of the mathematically based simulation models to faithfully and repeatedly mimic the actual biochemical/molecular changes indicates a constancy that argues against the concept that the actual biochemical/molecular cascades are sequences of random occurrences.

Thus, the occurrence of these mutations at specific atomic structure locations in molecules justifies a perspective that the mutations do not occur randomly among the molecule's atomic structure --- there is a plausible argument that the phototransduction cascade is executed by definitive "operational controls."

If the "operational controls" have not been identified, it necessarily follows that concepts involving randomness, as exemplified in this most extensively researched biological evolution organ, have no plausible basis of fact based on observations.

Perhaps the pursuing the nature of "operational controls" is comparable to an observation by Stuart Kauffman (77) when questioned about alternatives to natural selection"

I think self-organization is part of an alternative to natural selection. Let me try to frame it for you. In fact, it's a huge debate. The truth is that we don't know how to think about it. [emphasis supplied]

If "more detailed biochemical changes" and/or "more detailed molecular structures" cannot lead to an understanding of "operational controls" for a basic insight into evolution's "dark matter," is such research facing Kauffman's observation that the science doesn't know how to think about it?

Camazine (78) provides a perspective that forms a summary overview for this post's basic argument concerning a control mechanism behind the biochemical and molecular sequencing in the phototransduction cascade:

One of the great mysteries of biology is how the enormous morphologenic, physiological, behavioral, and cognitive complexity of an organism can be achieved with the limited amount of genetic information contained within the genome. It is inconceivable that the pattern of connections for each neuron in the brain could be genetically coded. Rather, there must exist special mechanisms for economizing on the amount of information that must be coded within the genes. Self-organization is such a mechanism. --- organisms can evolve mechanisms that rely on relatively simple sets of rules - algorithms economically encoded in the genome. [emphasis supplied]

It is arguable that Camazine's perspective is complementary to Carrol's "operational controls" as the "dark matter of the genome" and as such his "algorithms" are the mechanisms and processes that control the eye's phototransduction cascade.

Biochemical interactions and molecular change sequences are not "algorithms."

To this point, the treatment of phototransduction has focused on "operational controls" that are operational in current fully developed eye sustems.

But the perspective of undescribed "operational controls" extends into the origins aspect of phototransduction and as such implys critical implications for Darwinian randomness:

Inasmuch as self-organization is not yet well characterized, we still consider unexpected alterations to a system to be its characteristic function. But this differs from the neo-Darwinian concept of random alterations to the genetic information --- . With this gain in scope, we can now see clearly that selection occurs within frameworks at higher levels than the place where generativity is located. --- Natural selection disposes what self-organization proposes. (79) [emphasis supplied]

If the mechanisms and/or processes that control the staging of phototransduction's biochemical reactions and molecular-structure adjustments cannot be defined, then there is in fact no basis to argue that the sequential origins of the cascade elements occurred as a result of random development of those elements.

Considering the origin of rhodopsin, the first molecule in the cascade, as an example of knowledge of the origin of the constituents of the cascade:

Exactly how rhodopsin evolved originally is unclear. (80)

and more critically:

After all, molecular evolution obeys the same evolutionary principles that apply to anatomical structures. (80)

Thus, reversing the perspective: the evolution of anatomical structures obey the same evolutionary principles as molecular evolution.

Literature Cited:

33. Carrol, Sean B. Endless Forms Most Beautiful : The New Science Of EvoDevo. and The Making Of The Animal Kingdom. W. W. Norton And Company, Inc.

67. Gehring, W. J. New Perspectives on Eye Development amd the Evolution of Eyes and Photoreceptors. Journal of Heredity. 2005: 96 (3): 171-184.

68. Burns, Marie E. and Vadim Y. Arshavsky. Beyond Counting Photons: Trials and Trends in Vertebrate Visual Transduction. Neuron. Vol.49, 387-402. Novemver 3, 2005.

69. Kandel, Eric R. Principles of Neural Science. McGraw-Hill Companies. January 2000.

70. Sturm, Noel. Vitamin A and Vision. http://chemistry.gravitywaves.com/CHE452/16_Vitamin%20A%20and%20Vision.htm.

71. The Rhodopsin Cycle. http://education.vetmed.vt.edu/Curriculum/VM8054/EYE/RHODOPSN.HTM

72. Isayama, Tomoki, Anita L. Zimmerman and Clint L. Makino.The Molecular Design Of Visual Transduction. www.biophysics.org/portals/1/pdfs/education/Phototransduction.pdf

73. Cyclic guanosine monophosphate. http://en.wikipedia.org/wiki/Cyclic_guanosine_monophosphate

74. Casiday, Rachel and Regina Frey. "I Have Seen the Light!" Vision and Light-Induced Molecular Changes. http://www.chemistry.wustl.edu/~edudev/LabTutorials/Vision/Vision.html.

75. Mcbee, Joshua K. Krzysztof Palczeski, Wolfgang Baeht, and David R. Pepperberg. Confronting Complexity: the Interlink of Phototransduction and Retinoid Metabolism in the Vertebrate Retina. Progress in Retinal and Eye Research. Vol. 20, No. 4, pp. 469 to 529. 2001.

76. Kuska, Vladimir, Yoshikazu Imanishi, Matthew Batten, Krzysztof Palczewski and Alexander R. Moise. Retinoid cycle in vertebrate retina: experimental approaches and mechanisms of isomerization. Vision Research 43 (2003) 2959-2981.

77. Kauffman. S. Rethink Evo, Self-Organization Is Re4al. http://www.scoop.co.nz/stories/print.html?path=HL0805/S00052.htm

78. Camazine, Scott. Self-organizing Systems. web.mac.com/camazine/Camazine/Self.../Self-organization.pdf

79. Batten, David, Stanley Salthe and Fabio Boschetti. Visions of Evolution: Self-organization Proposes What Natural Selection Does. Biological Theory 3(1) 2008. Knorad Lorenz Institute for Evolution and Cognition Research.

80. Fishman, Ronald S. Evolution and the Eye. Archives Of Ophthalmology. Vol. 126 No. 11, November 2008.

81. Pattee, H.H. #TL20D: Causation, Control, And The Evolution Of Complexity. http://buildfreedom.com/tl/tl20D.shtml

Post 29: Evolution "processes"-WEit And Alternative Perspectives

2010-08-08T19:16:00.000-07:00

Post 28 contained the following quote from WEiT, and although concerned with the complexity and development of the flagellum, was assumed to be applicable to comparable complex animal organs:

We need only show that such a development, involving processes and constituents not unlike those we already know and can agree upon, is feasible. (page 138) [emphasis supplied]

This post picks up on WEiT’s “processes” concept and treats it in relation to how the term is used by evolutionary biology’s concerning the “effects” resulting from the execution of the “processes.”

The critical term in the foregoing WEiT quote to is “show” and is an essential aspect of this post’s analysis of whether or not the book, assumed to be representative of the biological evolution field in general, has in an empirical sense demonstrated the essential aspects of “show.”

Gregory (4) contains a table (Table 2), referred as “Examples from eye evolution,” that is assumed herein to be a reliable summary of processes that research on eye development has been documented by the field [bold emphasis supplied]

The table’s second column is apparently intended to illustrate “examples of processes from eye evolution” but in fact are “examples of results of eye processes involved in eye evolution.”

Table 2 Examples of some of the direct and indirect evolutionary processes that may be involved in the evolution of eyes

Process
Examples from eye evolution

Direct adaptive evolution
Gradual evolution of lens crystallin concentrations resulting in evolution of graded refractive index lenses in aquatic animals

Exaptation

  One structure has one function and takes on or switches to a new function in a new environment
The cornea, which has no refractive capacity in water, became the primary focusing structure after tetrapods moved onto land

The lens became far less important in image formation in terrestrial vertebrates and became specialized for accommodation
instead

  One structure has one function but becomes modified enough to allow a shift in function
Circadian organ in early chordates became modified sufficiently that it became capable of visual functions

An early protective, transparent layer of cells became sufficiently thickened and invaginated that it could begin serving as an early lens

  Two structures perform the same function but become differently specialized
Though both cell types were probably found in the distant bilaterian ancestor, ciliary photoreceptors became the dominant type in vertebrates whereas rhabdomeric photoreceptors came to predominate in most other animals (see also duplication and
divergence)

  A vestigial structure takes on new function
In vertebrates, rhabdomeric photoreceptors lost their microvilli and became retinal ganglion cells that function in circadian
entrainment rather than in vision

Duplication and maintenance of repetition
The compound eyes of arthropods are composed hundreds or thousands of repeated lens eyes called ommatidia

Duplication and divergence
Opsin genes duplicated and diverged to become r-opsins and c-opsins, along with specialization of rhabdomeric cells with r-opsins
and ciliary cells with c-opsins

In certain taxa, duplications and diversification of opsins to respond to different wavelengths of light allowed the evolution
of color vision

The rod cells of vertebrates are derived from cone cells, both of which are derived from a single ancestral ciliary photoreceptor

Gene sharing
Some lens crystallin proteins function both in the eye in light refraction and elsewhere in the body for other functions (e.g.,
cellular stress response)

Collage
The first photopigment was formed by the combination of a preexisting light sensitive molecule derived from vitamin A (which
became retinal) with a preexisting G protein-coupled receptor protein (which became the ancestral opsin)

The first “eye” arose by the combination of a photoreceptor cell with a pigment cell

During the evolution of complex camera-type eyes, various types of tissue that already existed (e.g., blood vessels, nerves,
muscles) were incorporated

Scaffolding
May apply to the evolution of phototransduction pathways or other relevant biochemical systems, but more data are required

Constraints, trade-offs, and historical contingency
Trade-off between resolution versus brightness in pinhole camera eyes

Trade-off between visual acuity versus size of compound eyes

Inverted retina in vertebrates

A narrow range of available wavelengths of sunlight is perceived in most animals, probably because eyes first evolved in water
which filters most wavelengths

Convergence
Lenses, irises, and various other components of camera-type eyes emerged independently in vertebrates and cephalopods

Parallel evolution
The same developmental or other genes may have been independently co-opted in different lineages (though homology is also
a possibility)

Process	Examples from eye evolution
Direct adaptive evolution	Gradual evolution of lens crystallin concentrations resulting in evolution of graded refractive index lenses in aquatic animals
Exaptation
One structure has one function and takes on or switches to a new function in a new environment	The cornea, which has no refractive capacity in water, became the primary focusing structure after tetrapods moved onto land
The lens became far less important in image formation in terrestrial vertebrates and became specialized for accommodation instead
One structure has one function but becomes modified enough to allow a shift in function	Circadian organ in early chordates became modified sufficiently that it became capable of visual functions
An early protective, transparent layer of cells became sufficiently thickened and invaginated that it could begin serving as an early lens
Two structures perform the same function but become differently specialized	Though both cell types were probably found in the distant bilaterian ancestor, ciliary photoreceptors became the dominant type in vertebrates whereas rhabdomeric photoreceptors came to predominate in most other animals (see also duplication and divergence)
A vestigial structure takes on new function	In vertebrates, rhabdomeric photoreceptors lost their microvilli and became retinal ganglion cells that function in circadian entrainment rather than in vision
Duplication and maintenance of repetition	The compound eyes of arthropods are composed hundreds or thousands of repeated lens eyes called ommatidia
Duplication and divergence	Opsin genes duplicated and diverged to become r-opsins and c-opsins, along with specialization of rhabdomeric cells with r-opsins and ciliary cells with c-opsins
In certain taxa, duplications and diversification of opsins to respond to different wavelengths of light allowed the evolution of color vision
The rod cells of vertebrates are derived from cone cells, both of which are derived from a single ancestral ciliary photoreceptor
Gene sharing	Some lens crystallin proteins function both in the eye in light refraction and elsewhere in the body for other functions (e.g., cellular stress response)
Collage	The first photopigment was formed by the combination of a preexisting light sensitive molecule derived from vitamin A (which became retinal) with a preexisting G protein-coupled receptor protein (which became the ancestral opsin)
The first “eye” arose by the combination of a photoreceptor cell with a pigment cell
During the evolution of complex camera-type eyes, various types of tissue that already existed (e.g., blood vessels, nerves, muscles) were incorporated
Scaffolding	May apply to the evolution of phototransduction pathways or other relevant biochemical systems, but more data are required
Constraints, trade-offs, and historical contingency	Trade-off between resolution versus brightness in pinhole camera eyes
Trade-off between visual acuity versus size of compound eyes
Inverted retina in vertebrates
A narrow range of available wavelengths of sunlight is perceived in most animals, probably because eyes first evolved in water which filters most wavelengths
Convergence	Lenses, irises, and various other components of camera-type eyes emerged independently in vertebrates and cephalopods
Parallel evolution	The same developmental or other genes may have been independently co-opted in different lineages (though homology is also a possibility)

The specific concepts discussed in this table are not germane to the principal theme of this post, but rather are intended to serve as a basis for continuing the examination of WEiT’s perception of showing “processes and their constituents” as interpreted by “mechanisms” and “processes” as understood by reasonably unbiased non-biological evolutionary sources.

A number of previous posts in this blog have essentially reduced the examination of WEiT’s evolution perspectives to questions concerning mechanism(s) and this post is intended to further establish the reality of those examination conclusions.

Thus, it is appropriate to establish the rationale this blog has relied on concerning these previous evaluations of WEiT’s perspectives, and for critiquing the concepts in the foregoing Gregory table.

Note that the right column of Gregory’s table, which herein is presumed to represent “processes,” uses terms such as “became,” “thickened,” “came to,” “derived,” “evolved,” and “arose” to describe changing organism properties.

Thus, these terms are the focus of the whether or not “show” has been achieved.

This same pattern of term usage was used in Lamb’s (64) table of vertebrate eye evolution which was critiqued in Post 4.

The explanation of “show” in relation to these terms requires a minimal venture into the philosophy of mechanism and its functional companion process.

In relation to the “process” terms used by Gregory in the foregoing table, the term “process” is of central import and is described as follows:

Process or processing typically describes the act of taking something through an established and usually routine set of procedures to convert it from one form to another. (From Wikipedia, the free encyclopedia.) [emphasis supplied]

A series of actions, changes, or functions bringing about a result: the process of digestion; (From: The Free Dictionary) [emphasis supplied]

From these two brief explanations of “process,” it can be argued that the concept essentially implies “changing” or “changing state of a condition.”

Since WEiT references “process” (however briefly in relation to the flagellum) and this blog’s continued stress on “mechanism,” and to avoid the appearance of using the concept to nitpick at WEiT’s use, it is necessary to preface this post’s arguments with a brief explanation of the “mechanism” concept. [emphasis supplied in all following Wikipedia quotes]

Mechanism Description

A mechanism is some technical aspect of a larger process or mechanical device, a part or combination of parts designed to perform a particular function. — Something resembling a machine in the arrangement and working of its parts. These also make a system or process work. [Wikipedia]

Mechanism Characterization

For example, one influential characterization of neuro- and molecular biological mechanisms is: mechanisms are entities and activities organized such that they are productive of regular changes from start to termination conditions (Peter Machamer, Lindley Darden, & Carl Craver 2000; 'MDC' hereafter). (From Wikipedia, the free encyclopedia.)

There are three distinguishable aspects of this characterization:

Ontic aspect

The ontic constituency of biological mechanisms includes entities and activities. Thus, the MDC conception postulates a dualistic ontology of mechanisms, where entities are substantial components, and activities are reified components of mechanisms. This augmented ontology increases the explanatory power of the MDC conception.

Descriptive aspect

Most descriptions of mechanisms (as found in the scientific literature) include specifications of the entities and activities involved, as well as the start and termination conditions. This aspect is mostly limited to linear mechanisms, which have relatively unambiguous beginning and end points between which they produce their phenomenon, although it may be possible to arbitrarily select such points in cyclical mechanisms (e.g., the Krebs cycle).

Epistemic aspect

Mechanisms are dynamic producers of phenomena. MDC emphasize activities, which are, essentially, causes that are reified. It is because of activities that the MDC conception of mechanisms is able to capture the dynamicity of mechanisms as they bring about a phenomenon.

From the foregoing brief descriptions of “mechanism,” it can be argued that the concept essentially implies “integrated working together.”

The concluding sections of Post 26 treated a logician’s perspective of “ground and consequent” as a different concept than “cause and effect” when analyzing relationships, and only addressed the relationship of “ground and consequent.”

The foregoing epistemic aspect of mechanism addresses the fundamental characteristic of “cause and effect” relationships — the aspect of “dynamic producers” and “dynamicity of mechanisms” — which means that “cause and effect” descriptions are based on dynamic relastionships between an initial condition and a consequential condition, i.e., essentially an empirically observed relationship between two conditions.

Thus, WEiT’s “shown processes” to a logician means that a mechanism relationship has been empirically demonstrated.

Maintaining a keen perception of the “dynamicity” of implied “cause and effect” relationships can reveal a great deal concerning WEiT’s (and other) explanations of why “it” is true.

“Mechanism” enters evolutionary development by integrating the various processes.(unidentified internet source) [emphasis supplied]

Logical assembly of components, elements, or parts, and the associated energy and information flows, that enables a machine, process, or system to achieve its intended result. (unidentified internet source)[emphasis supplied]

The theory of evolution is a body of interconnected statements about natural selection and the other processes that are thought to cause evolution, (65)[emphasis supplied]

In biology, a mechanism is part of an answer to a question about why some object or process occurred. Thus mechanism refers back from the object or process, along some
chain of causation. No description of mechanism is ever complete. For example, the mechanism of sunlight might include the rotation of the earth, the Earth’s orbit, the sun, nuclear reactions, heat, temperature, radiation emission, electromagnetic theory about propagation of light, formation of the solar system, etc. Compare this to the function of the object or process, which looks forward along some chain of causation to a goal or evolutionary success. (Wikipedia, the free encyclopedia.) (emphasis supplied)

The relationship of “process” and “mechanism” in relation to evolutionary biology is basically summarized in the following:

Obviously, some structures and molecular mechanisms need to be in place before it makes sense for others to evolve. In terms of eye evolution, it is clear that light sensitivity must have evolved to some degree before receptor-cell structures start to evolve, and receptor cells must, in turn, exist before s multi-cellular eye can be assembled. In this sequence of events, four different evolutionary processes come into play:

(i) evolution of molecular components,

(ii) evolution of cell structures,

(iii) evolution of cell types, and

(iv) evolution of organ shape—. (66) [paragraph restructuring supplied]

One of the products of foregoing processes, as part of the vertebrate eye, is that part of the eye called the “cup.”

A paper by Lamb et al. (64) contains a section entitled “The development of the vertebrate eye cup” in which they present Figure 4 captioned “Development of the vertebrate eye cup” that includes the following illustration.

In conjunction with the section’s textual description of the eye cup development sequence, the figure’s caption details the step-by-step development of the eye cup as follows:

a. The neural plate is the starting point for the development of the vertebrate eye cup.

b. The neural plate folds upwards and inwards.

c. The optic grooves evaginate.

d. The lips of the neural folds approach each other and the optic vesicles bulge outwards.

e. After the lips have sealed the neural tube is pinched off. At this stage the forebrain grows upwards and the optic vesicles continue to balloon outwards: they contact the surface ectoderm and induce the lens placode.

f. The optic vesicle now invaginates, so that the future retina is apposed to the future retinal pigment epithelium (RPE), and the ventricular space that was between them disappears. Developing retinal ganglion cells send axons out across the retinal surface. The surface ectoderm at the lens placode begins to form the lens pit. This section is midline in the right eye, through the choroid fissure, so only the upper region of the retina and the RPE are visible.

g. The eye cup grows circumferentially, eventually sealing over the choroidal fissure and enclosing the axons of the optic nerve (as well as the hyaloid/retinal vessels; not shown). The ectodermal tissue continues to differentiate and eventually forms the lens.

This figure is animated online (see Supplementary information S1.[emphasis supplied]

As “process” was earlier defined, these actions which transformed the structural state of the eye cup are examples of “processes” involved in developing the eye cup as a part of the overall eye structure development.

As “mechanism” was earlier defined, particularly by Nilsson (66), the “something” that was in action that controlled this development sequence in harmony with the myriad of companion development processes that were simultaneously occurring, was the “mechanism” controlling eye-cup development as part of the larger mechanism controlling eye development.

Posts 19 and 20 treated the question of such controlling mechanisms as the genetic toolkit that Carrol referred to as operational instructions for the tool kit.

For “mental image” generation, the most applicable feature concerning Lamb’s Figure 4 is the final line of text in the notation stating that the figure can be viewed in animation.
(here)

It is not clear to this blog what was the intended purpose of this animation — it is only an illustration wherein each step in the figure was spliced together with a sufficient number of intermediate steps (presumably based on empirical observations) and displayed by an image simulator that gives the impression of seamlessness (such as in a child’s “flip book”).

This artificial image simulator, with its obvious requirement of various “control” devices, is analogous to Carrol’s biological “operational instructions”

Thus, in short, the mechanism’s “operational instructions” that control the execution of the processes involved in eye-cup development were not explained.

Thus, regardless of the plausibility of the processes described in the developmental sequence as a recapitulation of the eye component origins, the paper’s description of the eye-cup developmental sequence does not explain “how” the eye cup developed, particularly in its stages of origin in the organ’s historical origins.

This post’s foregoing conclusion on the requirement of “mechanism operational controls” is given support by the following:

Although the exact history of any particular complex biological feature may never be fully worked out, biologists are confident that the mechanisms by which they arise can be – and to a growing extent, are — understood.(4) [emphasis supplied]

In Post 2, the ommatidium in the arthropod eye was used to base the following question: what controlled the development of each ommatidium component in such manner that all of the components were of the proper size and shape to “fit together” so as to accomplish the molding into the overall ommatidium?

For example, with illustration “f” in Lamb’s Figure 4 and the explanatory caption, there occurs the following:

The surface ectoderm at the lens placode began to form the lens pit.

Explanations of the operational instructions contained in the “processes” and “mechanisms,” such as with the “began” in the foregoing quote, should be sufficient to preclude the necessity of questions such as:

What controlled the development of the lens placode so that it invaginated in the observed direction and not in the opposite direction away from the developing eye cup?

Specifically, as the lense placode (in Figure 4 illustration f) developed, what controlled the size and shape of the developing lense such that it fit appropriately into the eye cup?

The observation that such fitting in fact occurs does not explain the nature of the “process” and “mechanisms” that controlled the fitting.

Did the eye socket and lens originate in conjunction with each other or did they develop in sequence, a general origin problem treated in Post 5 (gradual model) and post 6 (correlated progression model)?

Considering this perception of Lamb’s eye-cup development model as a likely example of other organ evolutionary development, WEiT’s “processes and constituents” about the flagellum and “those we already know and agree upon,” provides no support for the assertion that “it” is true and thus Darwin’s major tenets have been verified as an explanation of animal development from a common ancestor.

In commenting on a figure (not shown here) somewhat similar to Lamb’s Figure 4 and concerning such descriptions from extant animals, Gregory (4) provides an appropriate closing for this post.

Certainly, this series of changes does occur within the early development of vertebrate embryos — , though of course one must be very cautious not to overstate any similarities between ontogeny (development) and phylogeny (evolutionary history).

And:

Whereas some species do retain more primitive (ancestor-like) versions of particular organs and therefore provide information about how such simpler configurations could function, it is incorrect to compare modern species as though they represent actual steps in an evolutionary sequence of ancestors and dependents.

Literature Cited

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

64. Lamb, Trevor D, Shaun P Collin, and Edward N. Pugh. Evolution of the vertebrate eye: opsins, photoreceptors, retina and eye cup. Nature. Reviews. December 2007, Volume 8.

65. Douglas J. Futuyma, Evolutionary Biology, 2nd ed., 1986, Sinauer Associates, p. 15

66. Nilsson, Dan-Eric. The evolution of eyes and visually guided behavior. Phil. Trans. R. Soc. B (2009) 364, 2833-2847.

Post 28: Evolution "Changes": WEiT Perspective

2010-07-25T20:47:00.000-07:00

This post continues the examination of various WEiT perspectives that the book intends as support for the claim that “it” is true.

It was argued in Post 27 that the book’s use of “how,” in connection with a variety of biological evolution developmental phenomena, indirectly implicated the requirements to incorporate cause-and- effect and function as aspects of empirical evidence in scientific explanations.

This post focuses on WEiT’s use of the term “change,” in both its own perception and apparently in the perception of mainstream evolutionary biology.

This considerable list of WEiT’s use of “change” is deemed necessary for two reasons:

1. To avoid the appearance that this blog selected particular uses of the term “change” that, because of their context, created a biased view in order to support this post’s conclusions.

2. To represent the broad range of evolutionary biology concepts of “change” referenced by WEiT, i.e., from molecular-level “change” through all intermediate levels of change to species-level “change,” and thus, as intended in reason 1 above, to avoid the appearance that this blog “selected” a specific level of “change” to support its conclusions.

Thus, rather than a list to be sequentially “waded” through, there are levels of “change” examples for reference by particular “change” viewpoints that may become of interest (particularly to a WEiT proponent) as a result of this post’s conclusions. (emphasis supplied in all quotes).

Concerning genetic-level “change”:

This simply means that a species undergoes genetic change over time. (page 2)

— over many generations a species can evolve into something quite different, and those differences are based on changes in the DNA—. (page 2)

The most important is simple random changes in the proportion of genes caused by the fact that different families have different numbers of offspring. (page 13)

Natural selection, acting on coat color, has simply changed the genetic composition of a population, —. (page 117)

Second, some proportion of that variation has to come from changes in the forms of genes,—. (page 117)

Where does this genetic variation come from? Mutations — accidental changes in the sequence of DNA —. (page 118)

Most biologists define evolution as a change in the proportion of alleles —. (page 122)

— the proportion of different alleles can change over time entirely by chance. (page 122)

Both drift and natural selection produce the genetic change that we recognize as evolution. (page 123)

Genetic drift can change the frequency of alleles regardless of how useful they are to their carrier. (page 123)

Such random change in the frequency of genes over time is called genetic drift. (Page 123)

Many aspects of molecular evolution, then, such as certain changes in DNA sequence, may reflect drift rather than selection. (page 124)

Polyploid speciation differs from other types of speciation because it involves changes in chromosome number than changes in the genes themselves. (page 187)

Concerning species-level “change:"

Some, like horseshoe crabs and gingko trees, have barely changed over millions of years. (page 4)

The theory of evolution does not predict that species will constantly be evolving, or how fast they’ll change when they do. (page 4)

But if evolution meant only gradual genetic change within a species—. (page 5)

We should also be able to see cases of evolutionary change within lineages; that is, one species of animal or plant changing into something different over time —. (page 25)

What Darwin didn’t have were enough fossils to show clear evidence of gradual changes within species —. (page 26)

The record in the rocks confirms several predictions of evolutionary theory: gradual change within lineages —. (page 53)

Further, we shouldn’t expect to see more than small changes in one or a few features of a species —. (page 133)

Another factor making it hard to see real-time selection is that a very common type of natural selection doesn’t cause species to change. (page 133)

And sure enough, natural selection had changed flowering time in precisely the predicted way: after the drought, plants began to flower a week earlier than their ancestors did. (page 135)

— while Darwin did figure out how and why a single species changes over time (largely by natural selection) —. (page 170)

During biological speciation, populations change genetically to the extent that their members no longer recognize each other as mates —. (page 177)

And we should be able to see some species changing over time —. (page 18)

Concerning body-plan “change:"

It takes many generations to produce a substantial evolutionary change, such as the evolution of birds from reptiles. (page 4)

There are periods in which size doesn’t change much —. (page 30)

Unfortunately, we have no idea what selective pressures drove the evolutionary changes in these plankton and trilobites. It is always easier to document evolution in the fossil record than to understand what caused it, —. (page 32)

Breeders have virtually sculpted these dogs to their liking, changing the shade and thickness of their coats, —. (page 126)

If a species of birds for example, has evolved the optimum body size for its environment, and that environment doesn’t change, selection will act only on cull birds that are larger or smaller than the optimum. But this kind of selection, called stabilizing selection, won’t change the average body size: —. (page 133)

This is a staggering rate of evolutionary change — far larger than anything we see in the fossil record. (page 134)

Scott Carrol and his colleagues predicted that this host switch would cause natural selection for changes in beak size. — This is exactly what happened, with beak length changing by up to 25 percent in a few decades. (page 135)

Sure selection can change the beaks of birds, or the flowering period of plants, but can it build complexity? (page 136)

For anatomical traits, we can simply trace their evolution (when possible) in the fossil record, and see in what order different changes took place. We can then determine whether the sequence of changes at least conform to a step-by-step adaptive process. (page 138)

Certainly we know that there was enough time for organisms to have evolved — the fossil record alone tells us that — but was natural selection strong enough to drive such change? (page 140)

If evolution in the fossil record were much faster than in laboratory experiments or colonization events — both of which involve very strong selection — we might need to rethink whether selection could explain changes in fossils. (page 140)

Philip Gingerich at the University of Michigan showed that rates of change in animal size and shape during laboratory and colonization studies are actually much faster than rates of fossil change: —. (page 141)

The lesson, then, is that selection is perfectly adequate to explain changes that we see in the fossil record. (page 141)

A possible sequence of such changes begins with simple eyespots made of light-sensitive pigment, —. (page 141)

Concerning unspecified levels of “change:"

True, some change can occur very quickly. Populations of microbes have very short generations—. (page 4)

But when we’re talking about really big change, we’re usually referring to change that requires many thousands of years. (page 4)

When natural selection is strong —evolutionary change can be fast. (page 4)

This brings us to the last of evolutionary theory’s six points: processes other than natural selection can cause evolutionary change. (page 13)

The influence of this process on important evolutionary change, though is probably minor. (page 13)

Since there are fossil remains of ancient life, we should be able to find some evidence for evolutionary change in the fossil record. (Page 17)

We can now show continuous changes within lineages of animals: —. (page 26)This record gives an unambiguous picture of change, starting with the simple and proceeding to the more complex. (Page 26)

This pattern is quite common in fossils, and is completely understandable if the changes we see were driven by environmental factors such as fluctuations in climate or salinity. (Page 30)

Environments themselves change sporadically and unevenly, so the strength of natural selection will wax and wane. (Page 31)

Even a tiny advantage, so small as to be unmeasurable or unobservable by biologists in real time, can lead to important evolutionary change over eons. (page 124)

But if we can see selection causing small changes over just a few generations, then perhaps it becomes easier to accept that, over millions of years, similar types of selection could cause the big adaptive changes documented in fossils. (page 125)

This is easiest to do in microbes like bacteria, which can divide as often as once every twenty minutes, allowing us to observe evolutionary change over thousands of generations in real time. (page 128)

If we are to see natural selection at all, it must be strong selection, causing rapid change, —. (page 132)

To really see the power of selection, we must extrapolate the small changes that selection creates in our lifetime over the millions of years that it has really had to work in nature. (page 143)

All of these WEiT quotes use “change” that implies a “mechanism” responsible for converting one state of a biology condition into a new state of biological condition.

This “mechanism” is the critical feature on which rests the plausibility of WEiT’s explanations and examples that are presented as evidence that “evolution is true” and thus in support that all of Darwin’s main tenents have been verified.

If the “mechanisms” responsible for “change,” as implied in the biological changes cited in the foregoing quotes, cannot be empirically described, then WEiT has essentially explained nothing in terms of “how” the changes were executed.

In an example involving flagellar evolution in relation to the difficulty of explaining biochemical pathways involved in the development of complex characters, WEiT sets an example of what essentially constitutes “Mechanism causing a change” in the following:

We need only show that such a development, involving processes and constituents not unlike those we already know and can agree upon, is feasible. (page 138)

To this description associated with “mechanism” WEiT adds:

We can then determine whether the sequences of changes at least conform to a step-by-step adaptive process. (page 138)

Thus, to achieve plausible credibility, mechanisms that cause “change” must include explanations of “processes and constituents” and the “step-by-step sequences” involved in the process’s application of the constituents.

With this interpretation of “change,” WEiT’s consistent reliance on descriptions of completed stages in biological development sequences do not serve as evidence of the mechanism that are, however briefly acknowledged, conform to the book’s own requirements as evidence of “change.”

Furthermore, “changes” associated with the foregoing “species level,” “body-plan level,” and “unspecified level” quotes are actually “proximate changes,” which in themselves do not explain the “ultimate changes” which are associated with the genome level of complexity, as WEiT states in its discussion of the six components of the modern theory of evolution:

The first is the idea of evolution itself. This simply means that a species undergoes genetic change over time. That is, over many generations a species can evolve into something quite different, and those differences are based on changes in the DNA which originate as mutations. (page 3) [emphasis supplied]

Likewise, in discussion another of the six components, WEiT states:

Eventually the two populations would have evolved sufficient genetic differences that members of the different populations could not interbreed. (page 6) [emphasis supplied]

In the fifth part of the theory:

If individuals within a species differ genetically from one another, — . (page 11) [emphasis supplied]

And as a sort of summary for the foregoing:

This is genuine evolutionary change, demonstrating all three requirements of evolution via selection: variation, heritability, and the different survival and reproduction of variants. (page 128)

This includes not just body form and color, but the molecular features that underlie everything. (page 119)

Therein lies the criteria for judging the plausibility of WEiT’s referencing “change” in its explanation for the development of biological diversity — do any of WEiT’s statements concerning biological evolution “change” either contain or point to explanations that conform to the mechanism criteria specified above?

Of far greater importance: Does WEiT’s lack of mechanism explanation reflect the actual state of “change” as understood in the evolutionary biology field of endeavor?

Post 27: Evolution "Hows"- WEiT and Alternative Perspectives

2010-07-12T19:17:00.000-07:00

Within the variety of conceptual problems apparent in WEiT, some of which were briefly treated in the previous 26 posts, the concept most likely to reveal the failure of the book to plausibly establish “How” is its apparent "unorthodox" perspective concerning the term “how” in relation to the development of diversity in animal body plans.

An appropriate lead-in to this post’s focus on how the field expresses “how” is exemplified in Douglas Futuyma’s review (63) of the book:

—there still has not been a single book devoted to the simple task of showing readers the evidence for evolution and how it happens. We are fortunate that Jerry Coyne has exactly satisfied this need, with one of the very best and most important books on evolution for broad audiences in at least 50 years. [emphasis supplied]

In response to Futuyma’s perception of WEiT’s “how,” the following extensive quotes from the book are necessary to establish beyond reasonable doubt the main focus of this post: that WEiT used the term“how” as a reference to the causation of biological events as expressed in what this blog refers to as “Coyne’s model”, (here);which in effect implies the functional mechanisms responsible for the model’s development of animal diversity from “pre-existing traits” to the end point of “speciation”, which in reality are the varieties of extinct and extant animal body plans. All bold emphasis is supplied in all of the following quotes from WEiT.

These WEiT “hows” are segregated into three levels that infer (somewhat) a “mechanism level” of ultimate to proximate.

Hypothesis-level “hows:”

— Darwin didn’t really explain how new species arose. — Real understanding of how speciation occurs began only in the 1930's. (page 7)

First, in science, a theory is much more than just a speculation about how things are: ---. (page 15)

Similarly, the theory of evolution is more than just the statement that “evolution happened”: it is an extensively documented set of principles — I’ve described six major ones — that explain how and why evolution happens. (Page 15)

By predictions, I don’t mean that Darwinism can predict how things will evolve in the future. (Page 17)

Body-plan “hows:”

This is the fossil species Tiktaalik roseae, which tells us a lot about how vertebrates came to live on land. (Page 35)

My students had this chance when Neil brought a cast of Tiktaalik to class, passed it around, and showed how it filled the bill of a true transitional form. (Page 38)

But we no longer have to only imagine this step: we now have the fossils that clearly show how flying birds evolved. (page 39)

There is no need to describe this transition in detail, as the drawings clearly speak—if not shout–of how a land-living animal took to the water. (Page 49)

Specific-concept “hows:”

What we’re asking about here is not whether speciation happens, but how. (Page 178)

—the onus is not on evolutionary biologists to sketch out a precise step-by-step scenario documenting exactly how a complex character evolved. (Page 138)

The list flow is interrupted at this point for a comment: this WEiT statement borders on self incrimination in a book that claims to be an explaining the causation of evolution: Medical science, being in a leading position of research in discovering the role of epigenetics in causative mechanisms (treated in Post 21), will be relieved to know that science does not require step-by-step explanations of disease causation due to the difficulty of discovering causation and thus as a necessity for its findings to be viewed as plausible explanations.

But perhaps evolutionary biology is exempt from the difficulties of having to explain plausible causation for its hypotheses to be judged as plausible.

The interesting point is why WEiT would have to reach such a conclusion — the remaining sections of this post are intended to make the answer reasonably clear.

In particular, the failure to explain a step in the step-by-step mechanism, as will be evident at least in WET’s explanations if not in its “parent field,” constitute what this blog refers to as “WEiT’s missing links,” as titled in the “To” page.

—while Darwin did figure out how and why a single species changes over time (largely by natural selection), he never explained how one species splits in two. Yet in many ways this problem of splitting is just as important as understanding how a single species evolves. (Page 170)

How does this diversity arise from one ancestral form? (Page 5)

Natural selection is the most misunderstood part of Darwinism. To see how it works, let’s look at a simple adaptation: coat color in mice. (Page 116)

Selection is not a mechanism imposed on a population from outside. Rather, it is a process, a description of how genes that produce better adaptation become more frequent over time. (Page 117)

The theory of natural selection has a big job — the biggest in biology. Its task is to explain how every adaptation evolved, step by step, from traits that preceded it. (Page 119)

We may never have enough information to reconstruct the evolution of many traits, or even, in extinct species, to understand precisely how those traits functioned. (Page 120)

We’ll never be able to reconstruct how selection created everything—. (page 137)

Their evolution must be reconstructed in more speculative ways, trying to see how such pathways could be cobbled together from simpler biochemical precursors. (Page 138)

–we have to do more than explain how new traits arise — we must also explain how new species arise. (Page 170)

—we finally have a reasonably complete picture of what species are and how they arise. And we also have evidence for that process. (Page 170)

Under BSC, if you can explain how reproductive barriers evolve, you’ve explained the origin of species. (Page 174)

When considering the foregoing list of WEiT’s “how” explanations, the judgment criterion against which they must be compared is the Darwinian hypothesis that “descent with modification” in effect means “the descent of diverse body-plans” based on the undeniable evidence that a variety of body plans was/is the result of the “descent.”

The rest of this post involves evaluations of “principles” that are features of causative mechanisms that are intrinsic characteristics of the concepts that WEiT involves in its “how” explanations.

The foregoing of WEiT’s expressions of “how” are beyond reasonable doubt implications of causative mechanisms involved in the various expressions of “how” some developmental event occurred.

As such, the basic plausibility of whether or not the book actually provides evidence that supports it contention of why “it” is true, rests on whether or not some basic concepts of causation are addressed in connection with the “how” presentations.

As with the extensive quotes from WEiT in order to avoid mis-representation, and recognizing the tedium faced by a reader, an equally extensive set of quotes is considered necessary to avoid slanting or otherwise misrepresenting the basic concepts of principles that must be considered in causative explanations.

Spirkin, (61) in the paper “Dialectical Materialism” contains a chapter entitled “The System of Categories in Philosophical Thought,” under which is a section entitled “The Principle of Causality,” from which was extracted the following quotes.

(Please note before reporting this blog to the CIA, FBI, etc: As expressed by Lewontin, Gould, and Eldredge, referencing these materials is in the interest of their value as a heuristic. There is no intention of citing Spirkin’s materials as a dogmatic form of “social truth,” a statement of this blog’s politics, or their inclusion as a plan for a “Marxist plot” to overthrow the government via WEiT’s evolutionary philosophy.)

Likewise, the specific concepts treated herein are not necessarily presented as comprehensive or “the only way” in which WEiT should have explained the functional mechanisms of its “how” causes, but rather are intended to establish that “how” must be explained in terms of established principles of cause-and-effect relationships.

Each of the following paragraphs has direct implications to WEiT’s perception of “how.”

Part of their significance is that they are reasonably well divorced from biases that might be attributed to pro- or anti-Darwinism. (In all Spirkin quotes, bold text is supplied).

Causality is a genetic connection of phenomena through which one thing (the cause) under certain conditions gives rise to, causes something else (the effect). The essence of causality is the generation and determination of one phenomenon by another. In this respect causality differs from various other kinds of connection, for example, the simple temporal sequence of phenomena, of the regularities of accompanying processes.—A cause is an active and primary thing in relation to the effect. But “after this” does not always mean “because of this.”

The universality of causality is often denied on the grounds of the limited nature of human experience, which prevents us from judging the character of connections beyond what is known to science and practice. — The whole history of humanity, of all scientific experiments knows no exception to the principle of determinism.

The concepts of “cause” and “effect” are used both for defining simultaneous events, events that are contiguous in time, and events whose effect is born with the cause. In addition, cause and effect are sometimes qualified as phenomena divided by a time interval and connected by means of several intermediate links.

In the sciences, particularly the natural sciences, one distinguishes general from specific causes, the main from the secondary, the internal from the external, the material from the spiritual, and the immediate from the mediate, with varying numbers of intervening stages. The general cause is the sum-total of all the events leading up to a certain effect. It is a kind of knot of events with some very tangled threads that stretch far back or forward in space and time. The establishing of a general cause is possible only in very simple events with a relatively small number of elements. Investigation usually aims at revealing the specific causes of an event.

The specific cause is the sum-total of the circumstances whose interaction gives rise to a certain effect. Moreover, specific causes evoke an effect in the presence of many other circumstances that have existed in the given situation even before the effect occurs. These circumstances constitute the conditions for the operation of the cause.

For a cause to actually take effect there must be certain conditions, that is to say, phenomena essential for the occurrence of the given event but not in themselves causing it. Conditions cannot in themselves give rise to the effect, but the cause is also powerless without them.

One way of discovering casual connections is to study functional connections. — A functional connection is a dependence of phenomena in which a change in one phenomenon is accompanied by a change in another. — The functional approach is particularly useful when we are studying processes whose intrinsic casual mechanism is unknown to us. But when we wish to explain a phenomenon we have to ask what caused it.

The primary assumption for any scientific research has always been that all events of the natural and intellectual world obey a firm regular connection, known as the law of causality. Any field of knowledge would cease to be scientific if it abandoned the principle of causality.

A second section of Spirkin’s chapter on “The System of Categorical Thought” address what he refers to as “System and Structure” and is included herein as a followup to Spirkin’s linking of “function connections” with the discovery of “causation.”

The importance of these principles of “System and Structure” is to establish that WEiT’s use of “how” as a concept in reality is an expression of “function.” (all bold text is supplied)

The life of a structure manifests itself in its function, they condition each other. — . In the development of organisms, changes begin with the reorganization of an organ’s function under the influence of changing conditions of life, while its structure may survive for a time without any substantial modification. However, change of activity sooner or later leads to a change in structure. Functional disturbances in organs precede their morphological distortions. The contradiction between the organism’s new mode of life and its structure is resolved by modification in the latter.

— function organizes structure. The methods of morphology are subordinate to the methods of physiology. The function of sight organized the eye, while labour was responsible for the structure of the hand. But being an organized function, structure in its turn determines function.

An organic whole arises, is born, and dies together with its parts. It is an integral whole, with distinguishable parts. — The elements that make up the whole possess a certain individuality and at the same time they “work for” the whole...The whole is invisibly present, as it were, and guides the process of “assembly” of its elements, that is to say, of its own self.

For scientific analysis to be able to move in the right direction, the object must constantly occupy our consciousness as something whole. When we are investigation a whole, we break it down into its parts and sort out the nature of relation between them. We can understand a system as a whole only by discovering the nature of its parts. It is not enough to study the parts without studying the relationship between them and the whole. A person who knows only the parts does not yet know the whole. —An overabundance of particulars may obscure the whole. This is a characteristic feature of empiricism. Any single object can be correctly understood only when it is analysed, not separately, but in its relation to the whole. Each organ is determined in the mode of operation not only by its internal structure but by the nature of the organism to which it belongs. The importance of the heart can be discovered only by considering it as part of the organism as a whole.

The whole does not owe its origin to the synthesis of the parts that compose it. At the same time it is the whole that provides the basis for modification of existing parts and the formation and development of new ones, which, having changed the whole, help to develop it. So, in reality, we have a complex interaction between the whole and its parts.

The foregoing principles of cause-and-effect and structure-function were established reasonably free from specific biological evolution viewpoints, so the line of rationale needs to switch to a single paper by Longy (62) which is interpreted by this blog as expressing evolutionary biology concepts in a format sufficiently comparable Spirkin’s pure philosophical framework to bring biological reality to the principles (although Longy’s explanations are still based on”theory” rather than on empirical evidence).

In addition, Longy’s treatment of “causation” in relation to “natural selection” and “genetic drift” is particularly pertinent in light of WEiT’s assertion that:

“--- natural selection is the major engine of adaptation.” (page 223):

Natural selection remains the only process that can produce adaptation. (page 13)

Both drift and natural selection produce the genetic change that we recognize as evolution. (Page 123)

“— we know adaptations whose origin could not have involved natural selection,” (page 138)

“--- we can then determine whether the sequences of changes at least conform to a step-by-step adaptive process” (page 138)

As with Spirkin, Longy’s various examples and accompanying rhetoric are somewhat tedious to follow in order to bring the whole perspective into clear focus, which necessitates the extensive reliance on quotes in order to avoid, as clearly as possible, mis-representing his contentions.

The abstract of Longy’s paper sets the interpretation of the other quotes listed below (all bold text supplied):

To what do “natural selection” and “genetic drift” refer? To causes, as is usually thought? Or to mere statistical effects? The question arises because assessing causes faces specific difficulties when stochastic processes are concerned. In this paper, I establish that a central anti-causalist argument from Matthen and Ariew (2002) does not work, because selection doesn’t depend on chance (or unknown factors) in the manner that current analogies with games of chance suggest. I then explain how a clear understanding of how chance and biases are involved in natural selection supports one form of causalism, while every other form has indeed to be rejected.

Do “natural selection” and “genetic drift” name causes of biological evolution?— On the one hand are those who answer positively: — I will call them the causalists. On the other hand are those who argue that “natural selection” and “genetic drift” refer to mere statistical effects because of the role played by probabilities in contemporary evolutionary theory.

For the purposes of this post, the appropriate followup to the foregoing quotes, wherein the perspectives are defined in terms of the perspectives of “causalists” and “non-causalists (statistical effects),” is most clearly explained (in this blog’s opinion) in the section of the article that discusses the rationale of an imaginary “Mildred.”

So the causalist described here — appears to be a position implicitly endorsed intuitively by many, but a theory claimed by no one. Let us suppose, imaginary Mildred is defending explicitly such a theory. — imagine the train of thought of Mildred while looking at the deaths of two organisms, O1 and O2, who “otherwise very similar, differ in (vernacular ) fitness because O1 has better eye-sight than O2,” Mildred is supposed to know the two following facts:

C1: O2's bad eye-sight leads to its falling off a cliff. It dies and O1 survives.

C2: O1 is killed by a lightning strike — the difference of visual acuity was irrelevant to this event.

According to M&A [two authors whose work Longy frequently cites], Mildred will first remark that:

In the two cases, there is evolution since the genetic frequency in the population changes (the trait of good eye-sight which O1 possesses, advances somewhat in C1 and loses a little in C2.

Then, she will think accordingly that:

C1, however, seems to be a case in which the difference in vernacular fitness (the difference in eyesight) contributed to evolution, and C2 one in which a chance event thwarted the fitness difference that drives natural selection.

This will lead her to conclude that:

Natural selection is the cause of evolution in C1, and that it consists, over a longer period of time, of “predictable” (or fitness-biased) cases like C1, but that it excludes anomalous (or fitness-indiscriminate) cases like C2.

In the end, Mildred will even come to think that it is “plausible to say that something else — drift? Neutral selection? — is operation in C2

Longy sums up this scenario with the following:

Although this train of thought may appear rather convincing intuitively, M&A’s negative judgement is definitive. Such reasoning must be condemned, they say, because it “violates sound probabilistic thinking”. — Why does it violate sound probabilistic thinking? Because probabilistic causes entail an indeterminacy which goes both forward and backward, as the case of flipping coins shows. What makes it impossible to predict, if not probabilistically, the outcome of four tosses is also what makes it impossible to explain afterwards why the outcome was 4 heads, rather than, let’s say, 2 tails and 2 heads. The reason for this is simple: the outcome does not retroact on its cause. If the cause is probabilistic, it remains so no matter what the outcome. Once the tosses have occurred, there is no doubt about the outcome, of course, but the part supposedly played by chance (or unknown factors) has not changed. So, insofar as the probability is supposed to mirror the role of chance (or unknown factors), the outcome does not matter.

Longy follows the foregoing summation with the following concerning M&A:

The problem with M&A’s argument is not what they say about probabilistic causes, but how it applies to biological evolution. Of what sort are the probabilistic causes referred to when considering biological evolution? It does not really matter.

Then his further evaluation:

What is wrong with this line of reasoning? It ignores biases. The analogy between games of chance and biological evolution is misleading because it overlooks the question of biases. Now, selection is a biased stochastic process, as its identification with a discriminate sampling process stresses. There is selection when selective factors, such as good or bad eyesight, bias chance. — contrary to widespread opinion, fitness as well as any other probabilistic property may disappear from the causal explanation of an evolutionary outcome whereas probabilistic properties cannot be similarly eliminated when explaining the outcomes of game of chance.

Probabilities can be dispensed with in giving causal explanations of concrete cases of evolution because chance or unpredictability in evolution concerns the feature circumstances-encountered rather than the feature advantage. In other words, what is systematically dependent on chance or on unknown factors in evolution is whether a definite organism will meet circumstances in which having or not having a determinate character will be critical. Yet whether the possession of this character will be critical in some definite circumstance need not depend on chance.

In summary, the symmetry that exists with unbiased chance between prediction (telling the outcome from the cause) and retrodiction (telling the cause from the outcome) may disappear once the chance is biased and the question concerns the role played by biases. Chance (or unknown factors) acting on which circumstances an individual will encounter in his lifetime makes it indeterminate (or unpredictable if not in a probabilistic manner) when he will die and from what. It is, therefore, indeterminate (or unpredictable) whether the circumstances that will cause his death will give a decisive part to some selective factor (a bias).

These three paragraphs from Longy's paper constitute what kinds of factors WEiT's "hows" would have had to explain to justify that its perspective of natural selection and genetic drift were described in sufficient terms to support of its claim of "why it is true."

But ultimately, following additional examples, Longy concludes:

Let us see now how the type of argument put forth by M&A, and more generally by WALM [other authors whose findings he evaluates] helps clarify the issue of whether or not selection and drift deserve the status of causes, and finally demonstrates Mildred’s causalism to be the only defendable one. —WALM’s analyses also help make precise the idea that “selection” and “drift” refer to causes by making clear how causes contrast with statistical efforts relative to this particular issue.

Longy closes his paper with the following:

To sum up, the distinction between selection and drift that the causalist makes concerns not the casual role played by selective factors, but the type of statistical effect (at e-level) that results from a certain type of starting condition. It is in this sense that WALM draw a distinction between selection and drift understood as causes of evolution, and selection and drift understood as types of statistical effects.

And:

Agreeing with this distinction, I conclude that M&A’s argument demonstrates every form of e-causalism to be wrong, but not every form of i-causalism. However, a fully-fledged and coherent i-causalism position has yet to be formulated.

Without question, there are alternative perspectives of the principles involved in the cause-effect and structure-function mechanisms involved in “natural selection” and “genetic drift” causal mechanisms, but such alternative perspectives are not germain to the intent of this blog.

The key point to be made concerning the Spirkin/Longy principles is not in the plausibility of the details in their specific perceptions, but rather in the “fact” that in “real biology” there are either the same essential principles or comparable principles in action that must be addressed in explaining “how” biological variation actually occurred.

WEiT’s failure to frame its explanations of “how” evolution works is demonstrated in the following “how” claims that relate directly to Longy’s paper on natural selection and genetic drift.

One of WEiT’s most “in-depth” explanations of “how” natural selection “works” is contained on pages 116 and 117. “How” it “works” was entirely explained as coat color changes of mice. WEiT’s explanation was based solely on “effects” or the “consequences” of a variation “mechanism.” It requires no argument to conclude that “coat color” changes do not suffice as examples of “body-plan” variation (as extensively treated in Post 12), and indirectly as WEiT states on page 119, that natural selection must explain the evolution of “body form and color” (and molecular features).

Concerning the “genetic drift” portion of Longy’s paper, WEiT’s explanation of “how” drift works is contained on pages 122 through 124. The examples are blood types and the camel’s hump, with the blood type changes based on mutations changing the frequency of alleles. (Note WEiT’s comparison of this variation that “the “sampling” of genes is precisely like tossing a coin” — and compare with Longy’s interpretation). At least in his discussion of the “effects” of genetic drift, beyond the failure to address the mechanism’s involved, is the recognition that genetic drift cannot result in body-form variations, i.e., “a wing or an eye.”

The general principles addressed in this post are in part aspects of the “CORRELATION” and “CAUSE-EFFECT columns in the “KEY PRINCIPLES OF MECHANISM EXPLANATIONS” as depicted in the “WEiT’s MISSING LINKS” page of this blog.

In summary, the perspective that natural selection causes adaptation and adaptation causes evolution is can hardly be considered a sufficient explanation of “how” evolution works.

Considering the implications of the Longy paper, WEiT set out on a mission to explain “how” evolution works, that at least for the concepts of natural selection and genetic drift, the field of evolutionary biology has not successfully explained in terms of their functional mechanisms.

REFERENCES

61. Spirkin, A. The Basic Principles Of Dialectical And Historical Materalism. Moscow. Progress Publishers, 1971.

62. Longy, Francoise. Natural Selection as a Cause: Probability, Chance, and Selective Biases. Philosophy of Science Assoc. 21st Biennial Mtg (Pittsburgh, PA): PSA 2008 Contributed Papers.

63. Futuyma, Douglas J. What Everyone Needs To Know About Evolution. Trends in Ecology and Evolution Vol. 24, No. 7.

Post 26: Adaptation-Alternative Perspective

2010-06-06T19:36:00.000-07:00

In the closing remarks in Post 25, WEiT made reference that (1) each species is well adapted to its environment and (2) there are some cases of imperfect adaptation and are restated here because of their critical implications for this post’s arguments:

We should be able to find some cases of imperfect adaptation ---. (page 18) [emphasis supplied]

And natural selection makes each species well adapted to its environment. (page 94) [emphasis supplied]

Natural selection must also work with the design of an organism as a whole, which is a compromise among different adaptations. (Page 12) [emphasis supplied].

WEiT’s concept of the “well adapted” organism outproducing its competitors is based on the assumption, almost never specified, that an organism’s “well adapted” relationship with environmental conditions remains in effect, i.e., remains in a stable environmental/organism relationship, for a sufficient period of time for the “well adapted” organism to outproduce its competitors and thereby achieve numerical superiority.

The object of this post is to construct an argument that such an assumption of adaptation stability is in fact not how the environment-condition/organism-welfare-needs relationship actually exists.

One of the two critical concepts in this post proceeds from the conclusion in Post 24, that environmental conditions during which biological organisms have reached their current state of morphological/functional diversity, has been in more-or-less continual change, and thus the reality of environmental change need not be re-hashed in this post.

The WEiT perception of a trait or species being “well adapted” seems to imply that a morphology/function at its origin (from genetic changes) is in harmony with the environmental conditions and remains in such stasis with the environmental condition for a sufficient length of reproductive time to achieve its numerical dominance over another morphology/function that exists in less harmony with environmental conditions during the same reproductive time (see page 51 concerning adaptation to sea life; page 11 concerning adaptation to cold; page 94 concerning adaptation to desert)

Such seems to represent the general perception of evolutionary biology and thus the following argument, assisted by two symbolic flowcharts, is based on two such assumptions:

1. The adaptation that promotes the “survival of the fittest” must remain in effect for some time period of sufficient length for the “fittest” consequence to be achieved.

2. The environmental conditions associated with the achievement of the “fittest” consequence will have continually changed during the achievement period .

Two symbolic flowcharts are illustrated below that are centered on WEiT’s concepts of “well adapted” and “not so well adapted” organisms.

Scenario 1: A “well adapted” (i.e., “good variant”) species/trait progressing through a period of unfavorable environmental “condition” changes in respect to its effect on the species/trait survival fitness.

Scenario 2: A “imperfectly adapted” or “less well adapted” (i.e., “bad variant”) species/trait progressing through a period of favorable environmental “condition” changes in respect to its effect on the species/trait survival fitness.

If the morphology/function relationships that are altered by changing environmental conditions, as depicted in the foregoing scenarios, is a reasonable representation of reality, then there are grounds to argue that the whole concept of adaptation “stasis” of sufficient time span to perform the consequences of an organism attaining superior numbers due to its “well adapted” trait, is not in fact the actual situation.

Based on the foregoing symbolic illustrations, this post argues that they are a more plausible interpretation of how the environmental/morphology-function relationship actually works than the “standard” interpretation as perceived by WEiT.

In short, the “fitness” status of an organism’s adaptive condition is more often in “less well adapted” state than in a “well adapted” state.”

The necessary question follows: what actual evidence, other than the two presumptions on which the symbolic illustrations were based, can this post provide to support its conclusion?

The answer: none.

And neither did WEiT provide actual evidence to support the traditional view, other than the same kind of assumptions used by this post.

The reality of the “no evidence” in WEiT’s perception of adaptation can be clearly articulated with one question: What are example mechanisms in which are described specific enviromental agents that act on specific organism agents (“traits” that culminate in the “most offspring produced”), between “well adapted” and “not so well adapted?”

A paper addressing what Roberta Millstein (60) referred to as “The Great Snail Debate,” which addressed “the best way to characterize the concepts of random drift and natural selection,” contained the following evaluation that is pertinent to the “adaptation models” as perceived by WEiT and this post:

The proper role of statistics in determining the relative effects of drift and selection plays a large role in this debate. However, even though the two camps disagreed on this issue, there is agreement on the necessity of determining the causal factors at play. More specifically, both camps sought to determine the critical factors in the environment that determined which variant properties of the organisms were relevant to surviving and reproduction —. Simple correlations were not sufficient; specific selection mechanisms, such as selection by predator or climatic selection, that identified the causal factors at work had to be proposed (ideally with evidence). Causality was at the heart of this debate, and at the heart of the concept of selection as understood by the disputants. [emphasis supplied]

Millstein introduced the article with the following quote that sums up the status of the foregoing observation:

The debate was also messy; disputants were forced to turn philosophical—.

And following a three point list that specified particular questions, Millstens observed:

These three areas are still under lively philosophical debate today, —.

At this point, a short venture into the arena of the logician is relevant: in terms of evidence to support an argument, there is a significant plausibility difference between what the logician calls “ground and consequent” and “cause and effect.”

Calling again on Millstein, the foregoing challenge to WEiT can refined as follows:

(Other conceptual debates are revealed here — for example, the question of whether the selective environment is “fine-grained” or “course-grained,” which is also a topic that has engaged philosophers in the present day —). [emphasis supplied]

“Simple correlations” are in the logicians perspective, “ground and consequent” relationships and are in reality little more that expressions that two features appear to have some sort of causative relationship.

WEiT’s treatment of the relationship between natural selection and adaptation goes into no greater depth than Millstein’s “simple correlations,” as briefly presented in the three examples listed above (i.e., sea life, cold, desert), and due to the lack of evidence as prescribed by Millstein, is an indisputable case of “ground and consequent” rather than the required “cause and effect.”

As treated in Post 24, variation in environmental influences on genetic variation is beyond reasonable question, and thus environmental variation is a continuous factor in natural selection’s effects on adaptation and as such must be incorporated in the quest to determine the critical factors in the environment that determined which variant properties of the organisms were relevant to surviving and reproduction . [italicized text from Millstein; emphasis supplied]

WEiT did not bring this challenge, nor a plausible explanation, to the reader’s attention

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

21. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

22. Valentine, James W. and David Jablonski. Morphological and developmental macroevolution: a paleontological perspective. Int. J. Dev. Biol. 47, 2003.

23. Valentine, James W. Late Precambrian Bilaterians: Grades and Clades.. Tempo and Mode in Evolution: Genetics and Paleontology 50 Years After Simpson. 1995.

24. 7. Arthur, Wallace. The origin of animal body pl;ans: A study in evolutionary developmental biology. Cambridge University Press. 1997 & 2000.

25. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

26. Newman, Stuart A. and Ramray Bhat. Dynamical patterning modules: s “pattern language” for development and evolution of multicellular form. Int. J. Dev. Biol. 53: 693-705 (2009).

27. Rokas, Antonis. The Origins of Multicellularity and the Early History of the Genetic Toolkit For Animal Development. Annu. Rev. Genet. 2008. 42: 235-51.

28. Newman, Stuart A. The Developmental Genetic Toolkit and the Molecular Homology-Analogy Paradox. Biological Theory. 1 (1) 2006

29. Knoll, Andrew H. and Sean B. Carrol. Early Animal Evolution: Emerging Views From Comparative Biology and Geology. (?????????)

31. Erwin, Douglas H. Disparity: Morphological Pattern And Developmental Context. Palaeontology. Vol. 50, Part 1. 2007.

32. Dyer, Michael A., Rodrigo Martins, Manoel da Silva Filho, Jose Augusto P. C. Muniz,

33. Davidson, Eric H. and Douglas H. Erwin. Gene Regulatory Networks and the Evolution of Animal Body Plans. Science. Vol. 311. 2006.

34. Newman, Stuart A. and Ramray Bhat. Dynamic patterning modules: physico-genetic determinates of morphological development and evolution. Phys. Biol. 5(2008)

35. Newman, Stuart A. and Gerd B. Muller. Morphological Evolution: Epigenetic Mechanisms. In: Encyclopedia Of Life Sciences. 2001.

36. Newman, Stuart A., Ramray Bhat and Nadejda V. Mezentseva. Cell state switching factors and dynamical patterning modules: complementary mediators of plasticity in development and evolution. J. Biosci. 34(1), January 2009, 000-000.

37. Newman, Stuart A. Developmental mechanisms: putting genes in their place. J. Biolsci. Vol. 27. No. 2. March 2002.

38. Origination and Innovation in the Vertebrate Limb Skeleton: An Epigenetic Perspective. J. Exp. Z00 (Mol. Dev. Evol.) 304B: 593-609. (2005)

39. Newman, Stuart A., Gabor Forgacs and Gerd B. Muller. Before programs: The physical origin of multicellular forms.

40. Erwin, Douglas H. and Eric H. Davidson. The last common bilaterian ancestor. Development 129, 3021-3022 (2002).

41. Newman, Mark. "A Mathematical Model for Mass Extinction". Cornell University. May 20, 1994. URL accessed July 30, 2006.

42. Raup, David M. Extinction: Bad Genes or Bad Luck? W. W. Norton and Company. New York. 1991. pp.3-6 ISBN 978-0393309270

43. Jirtle: In Pray, Leslie A. Epigenetics: Genome, Meet Your Environment. The Scientist. Volume 18, Issue 13/14. July 5, 2004.

44. Hughes, Andrew. Epigenetics. Connexions. cnx.org . 2003.

45. Genetics Science Learning Center. University Of Utah. Http://learn.genetics.utah.edu/content/epigenetics.2010.

46. Evolution Fairytale Forum. www.evolutionfairytale.com/forum/index.php?...

47. Watters, Ethan. DNA Is Not Destiny. discovermagazine.com/2006/nov/cover

48. Goldberg, Aaron D. C. David Allis, and Emily Berstein. Epigenetics: A landscape Takes Shape. Cell 128, Feb 23, 2007.

49.The Epigenetics Center. John Hopkins Medicine. The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System.

50. Balon, Eugene K. Evolution by Epigenesis: Farewell to Darwinism, Neo- and Otherwise. Rivista di Biology Forum 97. 2004. Pp. 269-312.

51. Singer, Emily. A Comeback for Lamarckian Evolution? Technology. MIT Review, Feb 2009.

52. Venkat, Chaya. Genes Sleeping on the Job. Epigenetics. November, 2004.

53. McManamy, John. A New Science Peels Away Another Layer Of The Genetic Onion. Epigenetics. Jan 2004/2008.

54. Futuyma, Douglas. Natural Selection: How Evolution Works. In: AnActionBioscience.org original interview. December, 2004.

55. Genetic Recombination. Http://en.wikipedia.otg/wiki/Genetic_recombination.

56. Easton, John. Inherited individual variations influence patterns of gene shuffling. EurekAlert. 31-Jan-2008.

57. Lewis-Rogers, Nicole, Keith A. Crandell and David Posada. Evolutionary analysis of genetic recombination. Dynamical Genetics. 49-78. 2004.

58. Wright, Barbara E. A Biochemical Mechanism for Nonrandom Mutations and Evolution. Journal of Bacteriology. Vol. 182, No. 11, p. 2993-3001. June 2000.

59. Loewe, Laurence. Genetic Mutation. Nature Education 1(1). 2008.

60. Millstein, Roberta L. Concepts of Drift and Selection in “The Great Snail Debate” of the 1950's and Early 1960"s. Descended from Darwin: Insights into the History of Evolutionary Studies, 1900-1970. Journal of the History of Biology. V-41, No. 2, June 2008.

Post 25: Adaptation-WEiT Perspective

2010-06-06T16:25:00.000-07:00

As with the concept of mutations, WEiT did not list adaptation as one of Darwin’s six components (page 3) and likewise did not delve into the concept with meaningful explanations other than examples.

From the standpoint of explanations, in the book's glossary, WEiT perceives adaptation as a consequence:

adaptation: A feature of an organism that evolved by natural selection because it performed a certain function better than its antecedents. (page 247) [emphasis supplied]

Elsewhere, WEiT described adaptation as follows:

—when we say that “evolution is true,” what we mean is that the major tenents of Darwinism have been verified. Organisms evolved, they did so gradually, lineages split into different species from common ancestors, and natural selection is the major engine of adaptation. (page 223) [emphasis supplied]

Natural selection remains the only process that can produce adaptation. (page 13) [emphasis supplied]

The processes involved in the achievement of adaptation, in WEiT’s perspective, are as follows:

Three things are involved in creating an adaptation by natural selection. First, the starting population has to be variable —. Second some proportion of that variation has to come from changes in the forms of genes, that is, the variation has to have some genetic basis —. The third and last aspect of natural selection is that the genetic variation must affect an individual’s probability of leaving offspring. (pages 117-118) [emphasis supplied]

The fundamental concept of adaptation, i.e., the relationship between environmental conditions and an organism's capacity to outproduce other organisms, is illustrated in the following symbolic figure.

In reference to the foregoing symbolic figure and as a lead-in to the following post, three WEiT quotes are particularly relevant:

We should be able to find some cases of imperfect adaptation ---. (page 18) [emphasis supplied]

And natural selection makes each species well adapted to its environment. (page 94) [emphasis supplied]

Natural selection must also work with the design of an organism as a whole, which is a compromise among different adaptations. (page 12) [emphasis supplied]

Ruling out the consideration of continuous "instantaneous" matching of environmental condition changes and instantaneous organism requirement changes, developmental timing and coordination of environment conditions (physical and chemical) and biological requirements (the organism's needs) become the critical factor in the WEiT perception of a "well adapted" organism outproducing, over a long period of time, its "not so well adapted" competitors.

Literature Cited

(not listed for this post)

Post 24: Random/Chance Variation-Alternative Perspective

2010-05-29T19:39:00.000-07:00

This post has two primary objectives that are basic for examining WEiT’s (and thus evolutionary biology’s) perception of random/chance in the development of morphological and/or functional variation:

1. To switch the “process setting” associated with random/chance variation from the natural selection phase of morphological/functional development to the origin phase in genetic change.

2. To describe circumstances that question whether WEiT (and evolutionary biology) has sufficient plausible evidence to assign random/chance to the mutation origin of variation.

For the present, it is assumed that the “dinosaur egg laid-feathered bird hatched” concept is sufficiently implausible to justify a generality that the development of morphological/functional variation in organisms involves a process that can be considered a stage-to-stage sequence.

The intent of this post is to examination the stage-to-stage sequence for the process’s implications on the random/chance view in the development of morphological/functional variation in evolutionary biology.

However, as a basis for evaluation, WEiT perhaps contains no better succinct expression of a basic concept of Darwin’s hypothesis (that incorporates the idea of random/chance in the origin and fixation of morphological/functional variation in new body plans) than contained in the following:

It’s no surprise, then, that Darwin began “The Origin” not with a discussion of natural selection or evolution in the wild, but with a chapter called “Variation Under Domestication” — on animal and plant breeding. He knew that if people could accept artificial selection — and they had to, because its success was so obvious — then making the leap to “natural” selection was not so hard to accept. (Page 127) [bold emphasis supplied]

There’s really only one difference between artificial and natural selection. In artificial selection it is the breeder rather than nature who sorts out which variants are “good” and “bad.” In other words, the criterion of reproductive success is human desire rather than adaptation to a natural environment. (Page 127) [bold emphasis supplied]

We know that a process very like natural selection — animal and plant breeding — has taken the genetic variation present in wild species and from it created huge “evolutionary” transformations. (Page 143) [bold emphasis supplied]

The irony of Darwin’s deducing randomness/chance of artificial breeding processes being analogous to natural selection processes, as summarized in the first of the foregoing quotes, is that, according to current perceptions, the origin of morphological/functional variants in artificial breeding and natural selection in reality result from the same process — genetic recombination which is non-random.

These perceptions by WEiT provided the motivation for the preface of this blog that the book inadvertently provides a framework on which to base arguments contrary to its argument that Darwin’s hypothesis is “true,” particularly the concept that biological evolution occurred solely by random genetic changes.

Although WEiT apparently positions the critical determining actions of evolution variation, the “good/bad” concept of randomness, at the “good/bad” natural selection stage in the development and fixation of morphological/functional variations, the following statements position the origin of morphological/functional “good/bad” alternatives at the gene modification stage of the development/fixation process:

Where does this genetic variation come from? Mutations — accidental changes in the sequence of DNA—. (page 118) [emphasis supplied]

— the raw materials for evolution — the variations between individuals — are indeed produced by chance mutations. (Page 119) [emphasis supplied]

Such random change in the frequency of genes over time is called genetic drift. (Page 123) [bold emphasis supplied, underline by WEiT]

It is to be stressed that in these foregoing quotes WEiT specifically assigns the originating process(es) of variation to genes and as such constitutes the raw materials for evolution.

From WEiT’s positioning of origin of mutations, and thus the origin of morphological/functional variation, the evolutionary biology field’s perception of how mutations operate in the biological evolution process is assumed herein to be summarized as follows by Futuyma (54), responding in support (presumably as a spokesman for the conventional wisdom of the science) to a question involving Gould’s “rewind the tape” randomness scenario with alternative biological evolution consequences, provides the initial framework upon which to build the argument in this post:

—first of all, random processes are involved in the evolutionary process. For example, the origin of new mutations: a lot of evolution is dependent on particular mutational changes in genes that were very, vary rare or unlikely, but that just happened at the right time, in the right species, in the right environment but it need not happen that way. So, there’s this unpredictably.—If the sequence of environmental changes were different, you would have a different evolutionary history, leading to entirely different organisms over time. (54) [emphasis supplied]

In the foregoing quote by Futuyma, the critical point for the purpose of this post is the claim that “it need not happen that way” if the “sequence of environmental changes were different.”

As addressed in the discussion below concerning the causative agents involved in shaping genetic recombination, Futuyma’s implication concerning the environment’s effect on biological evolution are appropriate, but not as support for randomness.

Also, Futuyma’s linkage of biological evolution’s development with environmental agents in reality defines a “cause-and-effect” relationship, and as such, doesn’t it then follow that biological evolution’s development had a cause and therefore was not random (unless it can be shown that environmental condition were random which leads to questionable perspectives).

Contained in WEiT’s perception of mutations as the “raw materials for evolution” is a second critical element (in addition to random/chance as treated in Post 23) concerning the genetic processes involved in the origin of morphological/functional variations — the process of genetic recombination which is not mentioned in the book.

Since WEiT did not include the concept of genetic recombination as a process involved in the origin of morphological/functional variation, there are no specific points to directly address, thus this post will evaluate genetic recombination’s role in the origin of morphological/functional changes in terms that refute WEiT’s perception that randomness or chance is a “true” concept in Darwin’s hypothesis.

As expressed in the following quotes, it is beyond rational argument not to accept the concept of genetic recombination as a process (and as perceived by a credentialed representation of evolutionary biologists, likely “the” major process) in the origin of morphological/function variation by genetic change .

The shuffling of genes brought about by genetic recombinations is thought to have many advantages, as it is a major engine of genetic variation—. (55) [emphasis supplied]

Genetic recombination is a fundamental process, at the core of reproduction and evolution — yet we know very little about where it occurs or why there is so much variation among individuals in this important process — now, — we know where it occurs. Understanding where it happens provides us with important clues as to how it happens, how is regulated and what the mechanisms are that control this essential biological phenomenon. (56) [emphasis supplied]

Recombination is one of the key evolutionary processes shaping the architecture of genomes. Quantifying the effect of recombination is crucial to our understanding of how genetic diversity is generated and maintained in populations. — Ignoring the occurrence of recombination may influence the analysis of genetic data and the conclusions derived from it. (57) [emphasis supplied]

The most important sources of new genetic variants come from mutation and the novel combination of existing alleles through recombination. (57) [emphasis supplied]

It is beyond speculation concerning the genetic recombination concept’s relation to random/chance origin of morphological/functional variations, as described in the following perceptions of the concept’s non-randomness.

There is an abundance of evidence suggesting meiotic homologous recombination events are not distributed evenly throughout prokaryotic or eukaryotic genomes — . Rather, there are regions of elevated recombination known as recombination hotspots that are interleaved with regions that experience little or no recombination, referred to as warm and coldspots. Descriptions of linkage disequilibrium (LD) patterns have focused on identifying regions or blocks of low and high haplortype diversity. Regions exhibiting LD and thus lower diversity are assumed to represent nucleotide blocks that have historically undergone recombinations infrequently or not at all; whereas, regions with little or no LD and higher diversity are speculated to represent hotspots for recombination. (57) [bold emphasis supplied-underlining by source]

Relevant to the development of “hotspots” in considering the general concept of random/chance changes across the genome, the phenomenon of what appears to be historically undergone recombinations is a critical feature in eye development as discussed below.

Futuyma’s generalized reference to “if sequence of environmental changes were different” is a parallel concept to a “historical record of recombination interpretation” as termed by Wright in the following:

The structure of a gene is a distillate of its history, and the mutations that may occur in a gene are determined by the succession of environments in which that gene and its ancestors existed since the beginnings of life. The environment prevailing at the time mutation takes place is only a component of the environmental complex that determines the mutation. The definitions of directed and random that are appropriate in the above context are neither relevant nor useful, however, when discussing mechanisms of evolution. (58) [emphasis supplied]

This interpretation is the “cause-and-effect” process treated earlier in this post and is the primary basis for the argument that genetic changes resulting in morphological/functional variation actually are determined by other that random/chance.

The essential question is posed by Wright in terms of genetic “destabilizing” which is necessary for changes to occur:

What are the DNA-destabilizing processes operative in stressed, nongrowing organisms forced to mutate before they can continue to multiply? Mechanisms must have evolved in starving cells to stimulate metabolic changes and mutations that facilitate adaptation to new circumstances. (58) [emphasis supplied]

Wright also provides an essential argument for this post:

The definitions of directed and random that are appropriate in the above context are neither relevant nor useful, however, when discussing mechanisms of evolution. (58) [emphasis supplied]

Wright involves the concept of mechanism as follows:

However, the idea that mutations are random can be regarded as untrue if one considers the fact that not all types of mutations occur with equal probability.. Rather, some occur more frequently than others because they are favored by low-level biochemical reactions. — Mutation rates are usually very low, and biological systems go to extraordinary lengths to keep them as low as possible, mostly because many mutational effects are harmful. (59) [emphasis supplied]

— mutations occur preferentially in ssDNA and in unpaired and mispaired bases—. Other kinds of evidence also supports a role for secondary structures as precursors of mutations. Many insertion mutations — can best be explained if the other strand of a predicted transient stem were used as a template for DNA synthesis prior to replication. The fact that mutations are grouped closely together much more frequently than could occur by chance implicates a single initiating event (structure). — these investigations are but a small fraction of an enormous literature providing compelling evidence that the sequence-dependent secondary structures created and stabilized by supercoiling are precursors to mutations. (58) [emphasis supplied]

Evolution depends upon events that enhance mutation rates, thus increasing the supply of variants from which the fittest are selected. Therefore, the word mechanism in the present context will refer to the circumstances affecting mutation rates. That any DNA-destabilizing event will increase mutation rates is axiomatic. (58) [emphasis supplied]

As discussed above, background mutations are sequence directed and not random in the sense that they occur in bases made vulnerable by virtue of their particular location within specific DNA sequences, such as tandem repeats, or the unpaired and misplaced bases of stem-loop structures. (58) [emphasis supplied]

The eye development sequence as treated in Post 4 provides a “model” for relating the random/chance and genetic-recombination concept to reasonably plausible conclusions.

The eye development sequence, as presented, is a record of the historic accumulation of multiple gene changes that culminated in the morphology and function currently observed in the camera-lens eye.

Each of the 24 development stages, as described in the original literature, is a development stage during which the multiple changes in multiple genes established a morphological/functional structure upon which next development stage added an addition layer of morphological/functional variation.

There are two non-randomness implications associated with these development stages.

It is self-evident that there was an integrated set of multiple genes changes that were involved in shaping the morphological/functional characteristics of the new variants (addressed in Post 4 as the myriad of non-mechanism-specific changes) that had to mesh in perhaps countless ways with the prior development stage in order to maintain the morphological/functional pattern of development.

Thus, it is self-evident that the genetic changes involved in the new morphological/functional variants at each stage of development were not randomly distributed across the animal’s genome but rather occurred in association with the genetic changes that had occurred previously, i.e., the “recombination hotspots.”

Furthermore, unless the eye development sequence is an anomaly in the development of morphological/functional variants in other “body parts” (for example the associated eye lids, signal conducting nerves, eye socket, etc, etc, etc) the non-random eye genetic-change sequences process would also apply to other co-developing structures and as such there would be no evident genetic-change process which can be attributed to the concept of randomization or chance.

The second implication associated with the randomness concept involves WEiT’s perspective of “good” and “bad” variants being made available (by mutations) for natural selection to act on.

According to the “good/bad” perspective at each development stage for natural selection to act on, each of the eye development stages must have produced least one “bad” variant.

Thus, the question: could WEiT have presented observed evidence concerning the morphological/functional description of the “bad” variants?

The answer to this question needs no belaboring — there are no such observations and thus neither WEiT nor the conventional wisdom of evolutionary biology can respond with anything more plausible than suppositions that “the theory” requires the existence of “bad” variants.

The “bottom line” for this post: It is self-evident that each new stage involved in the morphological/functional stages in the eye development sequence had to exhibit morphological/functional aspects that “fit” the previous stage’s morphological/functional aspects.

As such, it is plausibly arguable that this sequence “fits” is an example of the “preconditioning of genetic change” that is implied in the genetic recombination concept and as such has no random or chance involvement.

The question is thus: has evolutionary biology described what was/is the mechanism(s) that accomplished this “preconditioned fit” — how did/does the mechanism work, the “operational instructions” as treated in Post 20, and as challenged by WEiT:

How, for example, can we determine whether mutations were mere accidents in DNA replication—. (page 137) [emphasis supplied]

WEiT’s explanations of “how” it was accomplished fall short of credibility, to put it mildly.

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

21. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

22. Valentine, James W. and David Jablonski. Morphological and developmental macroevolution: a paleontological perspective. Int. J. Dev. Biol. 47, 2003.

23. Valentine, James W. Late Precambrian Bilaterians: Grades and Clades.. Tempo and Mode in Evolution: Genetics and Paleontology 50 Years After Simpson. 1995.

24. 7. Arthur, Wallace. The origin of animal body pl;ans: A study in evolutionary developmental biology. Cambridge University Press. 1997 & 2000.

25. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

26. Newman, Stuart A. and Ramray Bhat. Dynamical patterning modules: s “pattern language” for development and evolution of multicellular form. Int. J. Dev. Biol. 53: 693-705 (2009).

27. Rokas, Antonis. The Origins of Multicellularity and the Early History of the Genetic Toolkit For Animal Development. Annu. Rev. Genet. 2008. 42: 235-51.

28. Newman, Stuart A. The Developmental Genetic Toolkit and the Molecular Homology-Analogy Paradox. Biological Theory. 1 (1) 2006

29. Knoll, Andrew H. and Sean B. Carrol. Early Animal Evolution: Emerging Views From Comparative Biology and Geology. (?????????)

31. Erwin, Douglas H. Disparity: Morphological Pattern And Developmental Context. Palaeontology. Vol. 50, Part 1. 2007.

32. Dyer, Michael A., Rodrigo Martins, Manoel da Silva Filho, Jose Augusto P. C. Muniz,

33. Davidson, Eric H. and Douglas H. Erwin. Gene Regulatory Networks and the Evolution of Animal Body Plans. Science. Vol. 311. 2006.

34. Newman, Stuart A. and Ramray Bhat. Dynamic patterning modules: physico-genetic determinates of morphological development and evolution. Phys. Biol. 5(2008)

35. Newman, Stuart A. and Gerd B. Muller. Morphological Evolution: Epigenetic Mechanisms. In: Encyclopedia Of Life Sciences. 2001.

36. Newman, Stuart A., Ramray Bhat and Nadejda V. Mezentseva. Cell state switching factors and dynamical patterning modules: complementary mediators of plasticity in development and evolution. J. Biosci. 34(1), January 2009, 000-000.

37. Newman, Stuart A. Developmental mechanisms: putting genes in their place. J. Biolsci. Vol. 27. No. 2. March 2002.

38. Origination and Innovation in the Vertebrate Limb Skeleton: An Epigenetic Perspective. J. Exp. Z00 (Mol. Dev. Evol.) 304B: 593-609. (2005)

39. Newman, Stuart A., Gabor Forgacs and Gerd B. Muller. Before programs: The physical origin of multicellular forms.

40. Erwin, Douglas H. and Eric H. Davidson. The last common bilaterian ancestor. Development 129, 3021-3022 (2002).

41. Newman, Mark. "A Mathematical Model for Mass Extinction". Cornell University. May 20, 1994. URL accessed July 30, 2006.

42. Raup, David M. Extinction: Bad Genes or Bad Luck? W. W. Norton and Company. New York. 1991. pp.3-6 ISBN 978-0393309270

43. Jirtle: In Pray, Leslie A. Epigenetics: Genome, Meet Your Environment. The Scientist. Volume 18, Issue 13/14. July 5, 2004.

44. Hughes, Andrew. Epigenetics. Connexions. cnx.org . 2003.

45. Genetics Science Learning Center. University Of Utah. Http://learn.genetics.utah.edu/content/epigenetics.2010.

46. Evolution Fairytale Forum. www.evolutionfairytale.com/forum/index.php?...

47. Watters, Ethan. DNA Is Not Destiny. discovermagazine.com/2006/nov/cover

48. Goldberg, Aaron D. C. David Allis, and Emily Berstein. Epigenetics: A landscape Takes Shape. Cell 128, Feb 23, 2007.

49.The Epigenetics Center. John Hopkins Medicine. The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System.

50. Balon, Eugene K. Evolution by Epigenesis: Farewell to Darwinism, Neo- and Otherwise. Rivista di Biology Forum 97. 2004. Pp. 269-312.

51. Singer, Emily. A Comeback for Lamarckian Evolution? Technology. MIT Review, Feb 2009.

52. Venkat, Chaya. Genes Sleeping on the Job. Epigenetics. November, 2004.

53. McManamy, John. A New Science Peels Away Another Layer Of The Genetic Onion. Epigenetics. Jan 2004/2008.

54. Futuyma, Douglas. Natural Selection: How Evolution Works. In: AnActionBioscience.org original interview. December, 2004.

55. Genetic Recombination. Http://en.wikipedia.otg/wiki/Genetic_recombination.

56. Easton, John. Inherited individual variations influence patterns of gene shuffling. EurekAlert. 31-Jan-2008.

57. Lewis-Rogers, Nicole, Keith A. Crandell and David Posada. Evolutionary analysis of genetic recombination. Dynamical Genetics. 49-78. 2004.

58. Wright, Barbara E. A Biochemical Mechanism for Nonrandom Mutations and Evolution. Journal of Bacteriology. Vol. 182, No. 11, p. 2993-3001. June 2000.

59. Loewe, Laurence. Genetic Mutation. Nature Education 1(1). 2008.

Post 23: Random/Chance Variations-WEiT Perspective

2010-05-21T15:06:00.000-07:00

Other than natural selection, perhaps the most deeply imbedded and unshakable dogma by the adherents of Darwin’s hypothesis, and likewise perceived by WEiT, is that all morphological/ functional variations were/are the result of random or chance changes during the process(s) of establishing morphological and/or functional variation in biological organisms.

The purpose of this post is to summarize the basis of this concept to provide a platform for examining, in a following post, if there is an arguable implausibility in its basis for the science’s most basic dogma.

Thus, it is curious to say the least, that in a book whose central purpose is to present evidence in support of why Darwin’s hypothesis of biological change is “true,” there is a paucity of explanations dedicated to random or chance variations.

From the tone of WEiT’s treatment of this bedrock concept, the book apparently adopts the perception that randomness and/or chance are “facts” of Darwin’s hypothesis.

WEiT devotes one short segment containing the following explanations of what is meant by randomness/chance in the establishment of variation in organisms, which will be argued, is open to the most discrediting criticism of Darwin’s hypothesis in terms of the plausibility of why “it” is True:

On the basis of many laboratory experiments, scientists have concluded that mutations occur randomly. The term “random” here has a specific meaning that is often misunderstood, even by biologists. What this means is that mutations occur regardless of whether they would be useful to the individual. (Page 118) [bold emphasis supplied, underlined emphasis by WEiT]

These mutations occur willy-nilly, regardless of whether they are good or bad for the individual. (Page 119) [emphasis supplied]

Rather than calling mutations “random,” then, it seems more accurate to call them“indifferent”:—. (page 118) [emphasis supplied]

There is first a “random” (or “indifferent”) process — the occurrence of mutations that generate an array of genetic variants—. (page 118) [emphasis supplied]

Thus, in the foregoing perspective, randomness/chance applies to the ultimate fate of the mutation in the welfare of an organism.

WEiT thus apparently perceives that randomness/chance is only determined during a post-genetic phase of the variation establishment process (presumably during the phase of natural selection) when the variation proves to be “good” or “bad” for the organism.

The critical importance of the foregoing explanations of the role of randomness/chance in the establishment of morphological/functional variation in biological organisms is it's basis for the field's fundamental assertion that the evolution of biological organisms is a random or chance process.

This WEiT assertion, from an alternative perspective, is further examined in the following post, but WEiT provides an opening pointing to that post’s perspective thrust:

How, for example, can we determine whether mutations were mere accidents in DNA replication—. (page 137) [emphasis supplied]

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

21. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

22. Valentine, James W. and David Jablonski. Morphological and developmental macroevolution: a paleontological perspective. Int. J. Dev. Biol. 47, 2003.

23. Valentine, James W. Late Precambrian Bilaterians: Grades and Clades.. Tempo and Mode in Evolution: Genetics and Paleontology 50 Years After Simpson. 1995.

24. 7. Arthur, Wallace. The origin of animal body pl;ans: A study in evolutionary developmental biology. Cambridge University Press. 1997 & 2000.

25. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

26. Newman, Stuart A. and Ramray Bhat. Dynamical patterning modules: s “pattern language” for development and evolution of multicellular form. Int. J. Dev. Biol. 53: 693-705 (2009).

27. Rokas, Antonis. The Origins of Multicellularity and the Early History of the Genetic Toolkit For Animal Development. Annu. Rev. Genet. 2008. 42: 235-51.

28. Newman, Stuart A. The Developmental Genetic Toolkit and the Molecular Homology-Analogy Paradox. Biological Theory. 1 (1) 2006

29. Knoll, Andrew H. and Sean B. Carrol. Early Animal Evolution: Emerging Views From Comparative Biology and Geology. (?????????)

31. Erwin, Douglas H. Disparity: Morphological Pattern And Developmental Context. Palaeontology. Vol. 50, Part 1. 2007.

32. Dyer, Michael A., Rodrigo Martins, Manoel da Silva Filho, Jose Augusto P. C. Muniz,

33. Davidson, Eric H. and Douglas H. Erwin. Gene Regulatory Networks and the Evolution of Animal Body Plans. Science. Vol. 311. 2006.

34. Newman, Stuart A. and Ramray Bhat. Dynamic patterning modules: physico-genetic determinates of morphological development and evolution. Phys. Biol. 5(2008)

35. Newman, Stuart A. and Gerd B. Muller. Morphological Evolution: Epigenetic Mechanisms. In: Encyclopidia Of Life Sciences. 2001.

36. Newman, Stuart A., Ramray Bhat and Nadejda V. Mezentseva. Cell state switching factors and dynamical patterning modules: complementary mediators of plasticity in development and evolution. J. Biosci. 34(1), January 2009, 000-000.

37. Newman, Stuart A. Developmental mechanisms: putting genes in their place. J. Biolsci. Vol. 27. No. 2. March 2002.

38. Origination and Innovation in the Vertebrate Limb Skeleton: An Epigenetic Perspective. J. Exp. Z00 (Mol. Dev. Evol) 304B: 593-609. (2005)

39. Newman, Stuart A., Gabor Forgacs and Gerd B. Muller. Before programs: The physical origin of multicellular forms.

40. Erwin, Douglas H. and Eric H. Davidson. The last common bilaterian ancestor. Development 129, 3021-3022 (2002).

41. Newman, Mark. "A Mathematical Model for Mass Extinction". Cornell University. May 20, 1994. URL accessed July 30, 2006.

42. Raup, David M. Extinction: Bad Genes or Bad Luck? W.W. Norton and Company. New York. 1991. pp.3-6 ISBN 978-0393309270

43. Jirtle: In Pray, Leslie A. Epigenetics: Genome, Meet Your Envirinment. The Scientist. Volume 18, Issue 13/14. July 5, 2004.

44. Hughes, Andrew. Epigenetics. Connexions. cnx.org . 2003.

45. Genetics Science Learning Center. University Of Utah. Http://learn.genetics.utah.edu/content/epigenetics.2010.

46. Evolution Fairytale Forum. www.evolutionfairytale.com/forum/index.php?...

47. Watters, Ethan. DNA Is Not Destiny. discovermagazine.com/2006/nov/cover

48. Goldberg, Aaron D. C. David Allis, and Emily Berstein. Epigenetics: A landscape Takes Shape. Cell 128, Feb 23, 2007.

49.The Epigenetics Center. John Hopkins Medicine. The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System.

50. Balon, Eugene K. Evolution by Epigenesis: Farewell to Darwinism, Neo- and Otherwise. Rivista di Biology Forum 97. 2004. Pp. 269-312.

51. Singer, Emily. A Comeback for Lamarckian Evolution? Technology. MIT Review, Feb 2009.

52. Venkat, Chaya. Genes Sleeping on the Job. Epigenetics. November, 2004.

53. McManamy, John. A New Science Peels Away Another Layer Of The Genetic Onion. Epigenetics. Jan 2004/2008.

Post 22: Variations From Mutations-WEiT Perspective

2010-05-17T19:17:00.000-07:00

The central theme of this post is the continued examination of WEiT’s perspective concerning the mechanism(s) that originate the structural and functional variations that culminate in the development of new body plans.

Natural selection was treated as a non-candidate for variation origination in Posts 19 (Alternative Genetic Perspective), 20 (Alternative Epigenetic Perspective, and 21 (Alternative Medical Science Epigenetics Perspective.

This post switches the examination to the concept of genetic mutations which is introduced as an expansion of WEiT’s six components comprising Darwin’s hypothesis:

Evolution, Gradualism, Speciation, Common Ancestry, Natural Selection, and Non-selective Mechanisms.

WEiT then assigns genetic mutation to the “evolution” component as the “idea of evolution”:

The first is the idea of evolution itself. This simply means that a species undergoes genetic change over time. That is, over many generations a species can evolve into something quite different, and those differences are based on changes in the DNA which originate as mutations. (Page 3) [bold emphasis supplied, underlined text WEiT’s]

WEiT’s perspective of genetic mutation as the mechanism responsible for variation seems to be essentially encapsulated in the following:

Where does this genetic variation come from? Mutations – accidental changes in the sequence of DNA that usually occur as errors when the molecule is copied during cell division. Genetic variation generated by mutation is widespread: mutant forms of genes, for example, explain variation in human eye color, blood type, and much of our — and other species’ — variation in height weight biochemistry, and innumerable other traits. (Page 118) [emphasis supplied]

— the raw materials for evolution — the variations between individuals — are indeed produced by chance mutations. (Page 119) [emphasis supplied]

—some proportion of that variation has to come from changes in the forms of genes, that is, the variation has to have some genetic basis—. (page 117)

Most biologists define evolution as a change in the proportion of alleles (different forms of a gene) —. (page 122) [emphasis supplied]

For the purposes of this post, the following WEiT perspective implies that diversity arises from the act of species splitting, and thus it is assumed herein that WEiT is equivocating “diversity” with “differences” as expressed in the first of the three foregoing quotes from the book.

How does this diversity arise from one ancestral form? This requires the third idea of evolution: that of splitting, or, more accurately, speciation. (Page 5) [bold emphasis supplied, underlined text WeiT’s]

This quote captures the critical point stressed in this post: How does this diversity arise , more specifically, by what mechanism does diversity originate?

In relation to different body plans, WEiT states:

—speciation simply means the evolution of different groups that can’t interbreed — two populations of a single reptilian species — beginning top evolve slight differences from each other. Over a long time, these differences gradually grew larger. Eventually the two populations would have evolved sufficient genetic differences that members of the different populations could not interbreed. (Page 6) [emphasis supplied]

As additional background for evaluating the plausibility of WEiT’s perspective concerning the place of “species splitting/speciation” in the process of new body-plan development, species splitting was treated in Post 13 (Species Splitting-WEiT Perspective) and speciation was treated in Post 14 (Speciation/Transitional Species), and thus the linkage of “species splitting/speciation” as a mechanism involved in the origination of morphological and/or functional variation can be essentially ruled out.

However, it is not clear that WEiT restricts the origin of morphological and/or functional; variation to genetic mutation:

And selection has to mold these features in a particular way. First, it has to create them — most often gradually — step by step from precursors. (Page 119) [emphasis supplied]

Both drift and natural selection produce the genetic change that we recognize as evolution. (page 123) [emphasis supplied]

It’s not hard to accept the idea that natural selection could cause, say, the evolution of whales from land mammals over millions of years, —. (page 125) [emphasis supplied]

Selection is not a mechanism imposed on a population from outside. Rather, it is a process, a description of how genes that produce better adaptations become more frequent over time. (Page 117) [emphasis supplied]

The explanatory features of WEiT’s perspective of the relationship of genetic mutation to morphological and/or functional variation is for the most part captured in the foregoing contents of this post.

Thus, considering WEiT’s assignment of genetic mutation as “the” concept in Darwin’s hypothesis, the absence of additional explanation concerning the mechanism(s) behind the origin of morphological and/or functional variation is particularly critical for the book’s assertion that all of the components of Darwin’s hypothesis, as defined by WEiT, have been satisfactorily established as “true.”

Instead, WEiT is replete with discussions concerning the morphological and/or functional differences between that are observed in organs, organ systems, total organisms, or species.

It is beyond argument that the examples of differences are intended as WEiT's supporting evidence concerning the "mechanisms"of genetic mutations and thus support for why "it" is true.

But, regardless of the relationahip between observed morphological/ functional differences in organs/organ systems/organisms/species and their genetic composition, these examples are results of causative mechanism(s) --- in no way do the examples explain the mechanism(s) of variation origin ---they are the results of mechanism(s) and not explanations of how the mechanism(s) or process(es) actually create/created variation.

In essence, the arguments concerning the origin of morphological/functional variation as presented in Post 21, i.e., the epigenetic "operational controls" hovering over genetic expression, are fully applicable in concluding that WEiT's perceptions of genetic mutation/variability are not plausible explanations of the role that genes per se play in variation.

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

21. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

22. Valentine, James W. and David Jablonski. Morphological and developmental macroevolution: a paleontological perspective. Int. J. Dev. Biol. 47, 2003.

23. Valentine, James W. Late Precambrian Bilaterians: Grades and Clades.. Tempo and Mode in Evolution: Genetics and Paleontology 50 Years After Simpson. 1995.

24. 7. Arthur, Wallace. The origin of animal body pl;ans: A study in evolutionary developmental biology. Cambridge University Press. 1997 & 2000.

25. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

26. Newman, Stuart A. and Ramray Bhat. Dynamical patterning modules: s “pattern language” for development and evolution of multicellular form. Int. J. Dev. Biol. 53: 693-705 (2009).

27. Rokas, Antonis. The Origins of Multicellularity and the Early History of the Genetic Toolkit For Animal Development. Annu. Rev. Genet. 2008. 42: 235-51.

28. Newman, Stuart A. The Developmental Genetic Toolkit and the Molecular Homology-Analogy Paradox. Biological Theory. 1 (1) 2006

29. Knoll, Andrew H. and Sean B. Carrol. Early Animal Evolution: Emerging Views From Comparative Biology and Geology. (?????????)

31. Erwin, Douglas H. Disparity: Morphological Pattern And Developmental Context. Palaeontology. Vol. 50, Part 1. 2007.

32. Dyer, Michael A., Rodrigo Martins, Manoel da Silva Filho, Jose Augusto P. C. Muniz,

33. Davidson, Eric H. and Douglas H. Erwin. Gene Regulatory Networks and the Evolution of Animal Body Plans. Science. Vol. 311. 2006.

34. Newman, Stuart A. and Ramray Bhat. Dynamic patterning modules: physico-genetic determinates of morphological development and evolution. Phys. Biol. 5(2008)

35. Newman, Stuart A. and Gerd B. Muller. Morphological Evolution: Epigenetic Mechanisms. In: Encyclopidia Of Life Sciences. 2001.

36. Newman, Stuart A., Ramray Bhat and Nadejda V. Mezentseva. Cell state switching factors and dynamical patterning modules: complementary mediators of plasticity in development and evolution. J. Biosci. 34(1), January 2009, 000-000.

37. Newman, Stuart A. Developmental mechanisms: putting genes in their place. J. Biolsci. Vol. 27. No. 2. March 2002.

38. Origination and Innovation in the Vertebrate Limb Skeleton: An Epigenetic Perspective. J. Exp. Z00 (Mol. Dev. Evol) 304B: 593-609. (2005)

39. Newman, Stuart A., Gabor Forgacs and Gerd B. Muller. Before programs: The physical origin of multicellular forms.

40. Erwin, Douglas H. and Eric H. Davidson. The last common bilaterian ancestor. Development 129, 3021-3022 (2002).

41. Newman, Mark. "A Mathematical Model for Mass Extinction". Cornell University. May 20, 1994. URL accessed July 30, 2006.

42. Raup, David M. Extinction: Bad Genes or Bad Luck? W.W. Norton and Company. New York. 1991. pp.3-6 ISBN 978-0393309270

43. Jirtle: In Pray, Leslie A. Epigenetics: Genome, Meet Your Envirinment. The Scientist. Volume 18, Issue 13/14. July 5, 2004.

44. Hughes, Andrew. Epigenetics. Connexions. cnx.org . 2003.

45. Genetics Science Learning Center. University Of Utah. Http://learn.genetics.utah.edu/content/epigenetics.2010.

46. Evolution Fairytale Forum. www.evolutionfairytale.com/forum/index.php?...

47. Watters, Ethan. DNA Is Not Destiny. discovermagazine.com/2006/nov/cover

48. Goldberg, Aaron D. C. David Allis, and Emily Berstein. Epigenetics: A landscape Takes Shape. Cell 128, Feb 23, 2007.

49.The Epigenetics Center. John Hopkins Medicine. The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System.

50. Balon, Eugene K. Evolution by Epigenesis: Farewell to Darwinism, Neo- and Otherwise. Rivista di Biology Forum 97. 2004. Pp. 269-312.

51. Singer, Emily. A Comeback for Lamarckian Evolution? Technology. MIT Review, Feb 2009.

52. Venkat, Chaya. Genes Sleeping on the Job. Epigenetics. November, 2004.

53. McManamy, John. A New Science Peels Away Another Layer Of The Genetic Onion. Epigenetics. Jan 2004/2008.

Post 21: Natural Selection: Alternative Medical Science Epigenetics Perspective

2010-05-01T20:51:00.000-07:00

The principal purpose of this post is to describe the apparent distinction between the current cause-and-effect structure of molecular relationships associated with epigenetics and the likely structure of Carrol’s (33) “Dark Matter of the Genome: Operational Instructions for the Toolkit,” i.e., operational instructions that control epigenetic processes (treated in POSTS 19 and 20).

In the field of epigenetic research, some of the most comprehensive and in-depth understanding of epigenetic’s roles in controlling the morphological consequences of genes has come from the medical profession and associated disciplines.

As such, these findings may be considered to be relatively immune from the often slanted interpretations that can be leveled at perceptions associated with either pro-Darwinism or anti-Darwinism perceptions.

Thus, what might be referred to as the “epi-Darwinism” understanding of epigenetics, whose emphasis is largely involving human health, provide reasonably unbiased implications of the relationship of this growing branch of science on the concepts of Darwin’s concepts of organism morphological development.

It is not the purpose of this post to delve into the voluminous material that comments on the science of epigenetics, but it is necessary, to establish a base for the contentions presented below, to outline a brief view of what epigenetics is basically about.

Although explanations of known and proposed epigenetic mechanisms typically involve mind boggling complexity, the basic concept is simply expressed in the following illustration and supporting text:

Epigenetics is all about controlled access to the information stored in your genes; the ideal is sufficient order to keep things nice and tidy, but enough access to make the genetic information useful. —When a segment of DNA is tightly wound around a histone core, the genes present in that segment of DNA are locked up and not accessible. The DNA has to become slack, flopping around just a bit, before the genes it carries can be of any use. In other words, there has to be a way for the histone core to hold on tight to the DNA strands wrapped around it for storage purposes, and yet be able to let it go slack during times when the sell needs to consult the “how to” instructions stored in a given gene in that part of the DNA. (52). [emphasis supplied]

There are tiny little negatively charged fragments called acetyl groups. When they are attached to the histone core, some of the positive charge of the histone core is neutralized by them, and the DNA strand is held less tightly. Remove the acetyl groups and the histone core becomes more positive, and grabs on tight to the DNA strand. Adding acetyl groups is then the way of getting access to the genetic information on the DNA string and removing the acetyl groups is a way of making the genes unavailable. (52)

The processes described in the foregoing two citations are illustrated in the following figure:

The use of mechanical/electrical mechanisms as analogies to describe organic processes and mechanisms can be easily distorted but they can serve as a means to establish images that have familiar context.

Among the numerous analogies used to build mental contexts is the structure and function of the modern electro/mechanical computer.

Jirtle (43) states:

If you liken the genome to the hardware of a computer, Jirtle explains, then “epigenetics is the software ---” [emphasis supplied]

For purposes of extending Jirtle’s analogy, consider that the essential hardware components of a computer are collections of “chips” that are designed to convert pieces of “presented” information into different pieces of “converted” information, with this process involving numerous “chips” that perform different sorts of conversion which ultimately result in the production of a final piece of information.

The processes inherent in this sequence of information transformation are controlled by Jirtle’s “software.”

These computational conversions are actually the software that comprises Carrol’s “operational instructions,” but with one critical addition — the operator who controls, according to solution requirements, selection of the specific instructional software (operational instructions).

Thus, an expanded sequence of Jirtle’s analogy consists of the following:

1. An operator’s information to be generated;

2. The operator’s selection and execution of the software whose feature to activate the computer’s chips;

3. The software’s activation of the necessary chips;

4. The chips processing the information.

The question can then be posed: Which of these steps fits the information pattern currently represented by epigenetic research?

Hughes (44) establishes an appropriate bases for developing this discussion:

One of the most fundamental questions in biology is: how does functional diversity arise from genetic homogeneity? Multicellular organisms present apparent paradox: every cell in our body arises from a single – celled oocyte —the single, homogenous genetic precursor — but our bodies are composed of a myriad of radically and subtly different cells.

The following figure illustrates Hughes’ concept.

The following figure jumps from this caricature to a flowchart that illustrates the components and functions of the on/off switches in epigenetic processes (note: the specifics illustrated in this flowchart are not germane to the principal point to be stressed, i.e., that the flowchart represents the components and functions of the computer chip analogy).

This figure is frequently revised. It is based on the latest laboratory data, some of which is not yet published. The figure illustrates the genetic regulatory system that turns on the genes that control the construction of a tissue called the endomesoderm in sea urchins. The system controls a core of six genes that code for master regulatory proteins that eventually switch on scores of proteins that boast many more DNA switches. The chart shows how and when genes are used at very specific time and places. This Gene regulatory network (GRN) is like a computer program with sophisticated on/off switches that control the process. (45) [emphasis supplied]

The problem I see with gene regulation is a complicated interlaced system that is like a computer code or chemical engineering schematic. That changing one switch effects the flow of the whole system. Simply stated, changing just one switch would not be enough, the whole system has to be coordinated. In other words, the system has to be designed to work up front. (45) [emphasis supplied]

Although the foregoing figure’s caption refers to the flowchart as analogous to computer software, a more appropriate analogy is that the flowchart represents a computer’s “chips” and their integrated connections.

The various labeled boxes can be visualized, to a certain extent, as fixed-structure computational components,---chips.

The first of the foregoing two figures is more appropriately viewed as the computer software that, in caricature form, provides operational instructions to the battery of computer “chips,” defined as follows:

But genes themselves need instructions for what to do, and where and when to do it. A human liver cell contains the same DNA as a brain cell, yet somehow it knows to code only those proteins needed for the functioning of the liver. Those instructions are found not in the letters of the DNA itself but on it, in an array of chemical markers and switches, known collectively as the epigenome, that lie along the length of the double helix. These epigenetic switches and markers in turn help switch on or off the expression of particular genes. Think of the epigenome as a complex software code capable of inducing the DNA hardware to manufacture an impressive variety of proteins, cell types, and individuals. (47) [emphasis provided]

Notice that the endomesoderm’s flowchart caption contains a statement significant for the point to be made: that the model, i.e., the chip complement and function, is frequently revised as new features of process are discovered in laboratory experiments.

If the analogy that the endomesoderm flowchart is equivalent to the chips in a computer, then the further defining of the complement and function of the flowchart, via new discoveries, essentially represents further defining of the structure and function of the chips, and does not enter the realm of the "software" that controls the operation.

This perspective leads to the seminal question for this post: Doesn’t this chip-complement -function scenario represent the kind of information currently representing the descriptions of the epigenome?

If so, then current epigenetic research, for all of its remarkable discoveries, essentially represents further elaboration of the complement and function of the epigenetic chips.

Thus, the second question: Can continued detailed description of the complement and function of the epigenome chips lead to the description of the software that controls the activation of the chips?

This continued detailing of the chip structure is aptly envisioned as layers of complement and function.

Enter the science of epigenetics, which attempts to explain the mysterious inner layers of the genetic onion —. Epigenetics delves deeper into the onion involving “information stored in the proteins and chemicals that surround and stick to DNA. (53) [emphasis supplied]

The following is presented as a list of the functional features that have been identified in the epigenome chip.

The emerging dialectic of epigenetics, including the marks, writers, presenters, readers, and erasers, promises to be a rich conversation—. (48)

These are the chip functions that the software must control.

To the foregoing chip complement and functions, the following must be considered:

Despite these advances, most of the great questions in epigenomics remain to be solved. For example, is there really a histone code — a specific combination of posttransitional modifications in histones that specify gene function and that is copied during DNA replication? Although dozens of posttransitional modifications of histones have been identified, as well as their effect on gene expression, only some of their recognition and modifying proteins have been identified. We still have not identified a biochemical mechanism for propagating these modifications to daughter cells during mitosis. — we know comparatively little about how these epigenetic programs are maintained or modulated by the environmental cues and how these signals target the biochemical complexes regulating gene expression. (49) [emphasis supplied]

Thus, relating these epigenetic concepts to WEiT, what does the concept of operational instructions mean for WEiT’s concept of “major forms,” i.e., novelty body plans, being created by “species splitting?”

Epigenesis creates new phenotypes according to “instructions” given not only by the genome —. The genome works from programmatic information recorded as the “memory” of past environments, developments and their genetic assimilation, but the phenotype is formed by an interaction with the present environment, with the building activity adding developmental information to the instructions based on programmatic information —. Novelties appear only during epigenesis. (50) [emphasis supplied]

And finally, in relation to WEiT’s declaration that:

The theory of natural selection has a big job–the biggest in biology. Its task is to explain how every adaptation evolved, step by step, from traits that preceded it. This includes not just body form and color, but the molecular features that underlie everything. Selection must explain the evolution of complex physiological features—. (Page119) [emphasis supplied]

To which is added the following:

Now, when we say that “evolution is true,” what we mean is that major tenents of Darwinism have been verified. (Page 223) [emphasis supplied]

Epigenetics research has the following to say in connection to WEiT’s foregoing assertions:

But the research now makes it more plausible that these things may be real and may be based in molecular mechanisms. (51) [emphasis supplied]

The actual mechanism underlying these patterns on inheritance is somewhat mystifying to scientists. (51) [emphasis supplied]

These epigenetic mechanisms, at the least, call into question WEiT’s claim that “selection explains everything,” including the creation of “major forms.”

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

21. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

22. Valentine, James W. and David Jablonski. Morphological and developmental macroevolution: a paleontological perspective. Int. J. Dev. Biol. 47, 2003.

23. Valentine, James W. Late Precambrian Bilaterians: Grades and Clades.. Tempo and Mode in Evolution: Genetics and Paleontology 50 Years After Simpson. 1995.

24. 7. Arthur, Wallace. The origin of animal body pl;ans: A study in evolutionary developmental biology. Cambridge University Press. 1997 & 2000.

25. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

26. Newman, Stuart A. and Ramray Bhat. Dynamical patterning modules: s “pattern language” for development and evolution of multicellular form. Int. J. Dev. Biol. 53: 693-705 (2009).

27. Rokas, Antonis. The Origins of Multicellularity and the Early History of the Genetic Toolkit For Animal Development. Annu. Rev. Genet. 2008. 42: 235-51.

28. Newman, Stuart A. The Developmental Genetic Toolkit and the Molecular Homology-Analogy Paradox. Biological Theory. 1 (1) 2006

29. Knoll, Andrew H. and Sean B. Carrol. Early Animal Evolution: Emerging Views From Comparative Biology and Geology. (?????????)

31. Erwin, Douglas H. Disparity: Morphological Pattern And Developmental Context. Palaeontology. Vol. 50, Part 1. 2007.

32. Dyer, Michael A., Rodrigo Martins, Manoel da Silva Filho, Jose Augusto P. C. Muniz,

33. Davidson, Eric H. and Douglas H. Erwin. Gene Regulatory Networks and the Evolution of Animal Body Plans. Science. Vol. 311. 2006.

34. Newman, Stuart A. and Ramray Bhat. Dynamic patterning modules: physico-genetic determinates of morphological development and evolution. Phys. Biol. 5(2008)

35. Newman, Stuart A. and Gerd B. Muller. Morphological Evolution: Epigenetic Mechanisms. In: Encyclopidia Of Life Sciences. 2001.

36. Newman, Stuart A., Ramray Bhat and Nadejda V. Mezentseva. Cell state switching factors and dynamical patterning modules: complementary mediators of plasticity in development and evolution. J. Biosci. 34(1), January 2009, 000-000.

37. Newman, Stuart A. Developmental mechanisms: putting genes in their place. J. Biolsci. Vol. 27. No. 2. March 2002.

38. Origination and Innovation in the Vertebrate Limb Skeleton: An Epigenetic Perspective. J. Exp. Z00 (Mol. Dev. Evol) 304B: 593-609. (2005)

39. Newman, Stuart A., Gabor Forgacs and Gerd B. Muller. Before programs: The physical origin of multicellular forms.

40. Erwin, Douglas H. and Eric H. Davidson. The last common bilaterian ancestor. Development 129, 3021-3022 (2002).

41. Newman, Mark. "A Mathematical Model for Mass Extinction". Cornell University. May 20, 1994. URL accessed July 30, 2006.

42. Raup, David M. Extinction: Bad Genes or Bad Luck? W.W. Norton and Company. New York. 1991. pp.3-6 ISBN 978-0393309270

43. Jirtle: In Pray, Leslie A. Epigenetics: Genome, Meet Your Envirinment. The Scientist. Volume 18, Issue 13/14. July 5, 2004.

44. Hughes, Andrew. Epigenetics. Connexions. cnx.org . 2003.

45. Genetics Science Learning Center. University Of Utah. Http://learn.genetics.utah.edu/content/epigenetics.2010.

46. Evolution Fairytale Forum. www.evolutionfairytale.com/forum/index.php?...

47. Watters, Ethan. DNA Is Not Destiny. discovermagazine.com/2006/nov/cover

48. Goldberg, Aaron D. C. David Allis, and Emily Berstein. Epigenetics: A landscape Takes Shape. Cell 128, Feb 23, 2007.

49.The Epigenetics Center. John Hopkins Medicine. The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System.

50. Balon, Eugene K. Evolution by Epigenesis: Farewell to Darwinism, Neo- and Otherwise. Rivista di Biology Forum 97. 2004. Pp. 269-312.

51. Singer, Emily. A Comeback for Lamarckian Evolution? Technology. MIT Review, Feb 2009.

52. Venkat, Chaya. Genes Sleeping on the Job. Epigenetics. November, 2004.

53. McManamy, John. A New Science Peels Away Another Layer Of The Genetic Onion. Epigenetics. Jan 2004/2008.

Post 20: Natural Selection: Alternative Epigenetic Perspective

2010-04-06T15:12:00.000-07:00

This post has three objectives.

First, to present a brief summary of the evidence that forms the basis for the “epigenetic” rationale that the “genes only” concept of the genetic toolkit is not a sufficient stand alone mechanism and thus requires, as implied in the closing remarks in Post 19, “operational instructions” that in essence direct the activities of the toolkit’s complement of action-implementing features.

Second, to argue that evidence associated with the epigenetic concept as the controlling mechanism for the operation of the genetic toolkit does not qualify as the fundamental mechanism that controls the design of morphological elements in vertebrate limb development.

Third, to argue that the fundamental mechanism that controls the structure of morphological elements in vertebrate limb development negates WEiT’s perspective that natural selection, operating in species splitting, is the event that develops new body plans.

Epigenetic Implications On The Gene-Centered Toolkit
The central goal of epigenetic research has been to determine the step-by-step pattern of the genetic/molecular machine sequence.

Perhaps the clearest way to address the question of the toolkit’s “operation instructions,” herein interpreted as the toolkit’s “mechanism,” is summarized as follows:

If the origins of some of the gene machinery that makes us multicellular can be found in our unicellular relatives, how did it get there in the first place and what was its original function? (27) [emphasis supplied]

What kind of evolutionary process could rapidly generate a collection of morphologically distinct metazoan body plans from a common ancestor of annelids, molluscs, nematodes, arthropods, and chordates, while maintaining largely unchanged a core development toolkit? (28) [emphasis supplied]

The two foregoing quotes summarize in question form the fundamental rationale that there are “epigenetic” (i.e., beyond genes) mechanisms that are basically responsible for the diversity of morphological forms---body plans.

The role played by epigenetic mechanisms is clearly stated:

Epigenetic mechanisms are, to a great extent, the way in which molecular and genetic components perform their developmental roles. (38) [emphasis supplied]

In the discussion of their epigenetic perspectives on which much of the paper’s rational is based, there is the following key observations for the purposes of this post:

The collection of molecular-physical modules in effect constitutes a “pattern language” — for multicellular form. (26)

Development of the amimal body plan is controlled by large gene regulatory networks (GRNs), and hence evolution of body plans must depend upon change in the architecture of developmental GRNs. (33) [emphasis supplied]

We have further proposed that each pattern-language element is tied to a set of gene activities of the so-called developmental-genetic toolkit many of which pre-evolved the metazoa in single-celled ancestors. The elements of the pattern language, however, are not genes, gene products, or even merely gene networks. They are, rather, what we term dynamical patterning modules or DPM’s, in which a complex of the toolkit gene products mobilizes a mesoscale physical process. (26) [emphasis supplied]

In this view, networks of gene interactions regulate inherent system behaviors that depend on properties and mechanisms beyond the strictly genetic. (38) [emphasis supplied]

Newman Model Implications On Epigenetic Mechanism(s)
The paper selected for example argument herein is authored by Newman et al. (38) and is assumed to be a reasonable representation of the current perceptions associated with the epigenetic concept.

Newman et al. (38) use the development of the vertebrate limb as an example of the “toolkit’s” operational results—the product’s (i.e., new body plans) of the actual organic mechanisms or program that execute the genetic complement.

The paper initiates the limb development sequence that starts with “precartilage mesenchymal tissue” as follows:

We suggest that the bauplan of the limb is based on — the self-organizing properties of precartilage mesenchymal tissue are — the basis for its ability to generate regularly spaced nodules and rods of cartilage. —we propose that evolution refines skeletal templates generated by this process by mobilizing accessory molecular and biomechanical regulatory processes to shape the developing limb and its individual elements. (38) [emphasis supplied]

It is pertinent to establish the four segments of limb morphology that the authors include in their epigenetic vertebrate limb development concept:

For the forelimb of the chicken — this means the humerus of the upper arm is generated first, followed by the radius and ulna of the mid-arm, the wrist bones, and finally the digits. (38) [emphasis supplied]

Also key in the argument herein is the author’s additional categorization of the three limb segments.

This capacity to undergo qualitative morphological change as a result of quantitative changes in system parameters, seen in — the modeling of the normal developmental transition from stylopod (single upper limb bone to zeugopod (double mid-limb bones) to autopod, is a generic property of mechanisms based on reaction-diffusion instabilities. (38) (emphasis supplied)

A key consideration in the author’s conclusions concerning the control mechanism that guides the genetic toolkit’s processes in the development of the vertebrate limb lies in the conclusions that were derived from observations of mathematical programs.

As simplified as this system is relative to the cellular and molecular interactions in the actual developing limb, computer simulations of a set of equations of this complexity to determine the morphogen and condensation patterns it can produce is not feasible. It is possible, however, to use mathematical techniques to determine whether mathematical techniques to determine whether physically realistic solutions to these equations exist which correspond to nonuniform patterns of cell density. We have confirmed that this is indeed the case—. (38) [emphasis supplied]

Following this statement, the paper displays the mathematical equations that were used to generate the morphological consequences that were brought under various points of discussion related to the limb’s development sequence.

The model’s specific design and symbol representations are not pertinent for the purpose of this post, rather, the emphasis herein is on what the elements in the model are intended to be analogous to in the actual organic control mechanisms.

Likewise, this post is not concerned with the functions of the mathematical expressions per se, but rather with the implication that they point to the actual organic mechanism that controls the toolkits application to morphological developments.

Thus, regardless of its state of reality, the model is in effect a symbolic representation of the actual organic operating instructions that implement the toolkit’s components.

In the paragraph following the equation illustrations, the authors explain in some detail what function each of the equation’s symbols are intended to represent.

The implications associated with the functions of the mathematical symbols are sufficiently critical (for evaluating the state of evolutionary biology’s evidence concerning the mechanisms that control the development of new body plans via the toolkit components) to justify listing the entire paragraph as follows.

In these equations,

c, ca, ci, and R represent, respectively, the position- and time-dependent concentrations of FGF, TGF-β and the hypothesized inhibitor, and the density of mobile cells.

The J’s are reaction terms governing the production, and

the D’s are diffusion constants governing the transport, of these molecules, while

V2 and ∂=∂t are differential operators over space and time.

With the incorporation of the cell division rate r,

the fractions α, β, γ of the total mobile cell density R in the categories R1 (FGFR1- expressing), R2 (early FGFR2-expressing) and R'2 (FGFR2-expressing, fibronectin-secreting), and constants k and the k’s, this set of equations defines a streamlined network representing the core mechanism for spatiotemporally regulated chondrogenesis. [emphasis supplied

The emphasized action terms are in effect names for components that are the “operational instructions” for directing the actions of the toolkit’s genetic/molecular components.

The sought-after "operational instructions" are the organic counterparts of the mathematical sumbols and operators that set the genetic/molecular components to work.

The delineation of the actual organic controlling mechanisms of the toolkit is the explanation that evolutionary biology is seeking and must be described according to WEiT’s declaration:

The theory of natural selection has a big job–the biggest in biology. Its task is to explain how every adaptation evolved, step by step, from traits that preceded it. This includes not just body form and color, but the molecular features that underlie everything. Selection must explain the evolution of complex physiological features—. (Page119) [emphasis supplied]

The critical feature lies in the obvious conclusion that the mathematical model only represents the vertebrate limb’s sequential development as mathematically simulated by the sequential application of the toolkit’s genetic/molecular “tools.”

Neither the model nor the textual explanations identify or describe the "controlling instructions."

In addition, it can be argued that one of the model’s most significant failure to mimic the organic is the incompleteness of its computed morphological representation of the vertebrate limb.

The incompleteness of the model’s output in terms of morphological features is stated as follows:

While joints, i. e., discontinuities between the stylopod-, zeugopod- and autopod-like domains, or within the digit-like elements, do not appear in these particular simulations, slight changes in the parameter values in the core mechanism can produce such gaps. (38) [emphasis supplied]

This statement calls for several observations.

First, the “slight changes” to the model are essentially additional genetically based developmental sequences that are added to the genetic developmental sequences in the “jointless” version of the mathematics.

Second, the model’s resulting morphological structure only deals with the sequence of “bone” assembly and the number of “bones” in each step of the sequence, but not in the morphological or instructional specifics.

The morphological specifics and pattern of arrangement of the vertebrate limb are particularly relevant in terms of what morphological results the model produced.

The bones of the limb are discrete arrays of elements that individually differ in size and shape and vary in number in a discontinuous fashion between limb region, limb type, and species. (38) [emphasis supplied]

The critical aspect is the significant difference between the model’s morphological output of bone sequence and bone numbers in each sequence that have no size or form relationship to the associated bones in the actual morphological structure of the vertebrate limb size and shape.

Thus, the model contributes no evidence or other understanding of what/how the specific size and shape of the different bones are controlled, including the intricate articulations (the model’s discontinuities) that link the bone segments and form a functioning organ.

This problem is essentially comparable to the treatment of the arthropod ommatidium in Post 2 wherein the question was posed concerning what mechanism controlled the size and shape of the ommatidium’s individual components in their origin sequence so that they “fitted together” as an a continuously functioning organ.

Likewise, the “Newman et al. Model” provides no insight concerning the mechanism (Carrol’s “operational instructions ”) that controlled the sequential origin of the individual vertebrate limb bones sizes and shapes and their interrelated connective elements as specified below:

— evolution refines skeletal templates generated by this process by mobilizing accessory molecular and biomechanical regulatory processes to shape the developing limb and its individual elements. (38) [emphasis supplied]

In summary, the model does not identify the basic morphological mechanism(s) that control the development specific elements that comprise the vertebrate limb, but essentially represents more detailed developmental sequences in the process of the toolkit’s progressive development of the vertebrate limb in extant vertebrates.

In keeping with the basic thrust of this blog, until evolutionary biology constructs a definitive explanation of the toolkit’s actual organic “operational instructions,” there can be no plausible explanation involving the origin and development of the genetic/molecular toolkit or the toolkit’s “operational instructions,” regardless of the claim that:

--- this set of equations defines a streamlined network representing the core mechanism for spatiotemporally regulated chondrogenesis. (38) [emphasis supplied]

In terms of the mechanisms discussed above, we suggest the following scenario for the origination and subsequent refinement of the vertebrate limb. (38) [emphasis supplied]

This post’s foregoing summary is effectively confirmed by the following:

We do not have enough information at present to say that the hypothesized core processes and related “bare-bones” mechanism were indeed the originating mechanism by which limbs first appeared in vertebrate ancestors approximately 400 million years ago. (38) [emphasis supplied]

This conclusion essentially relegates to speculation WEiT’s evidence that "evolution is true" based primarily on body-plan diversification via species splitting.

WEiT’s Natural Selection Implications
As for WEiT, the essential perspective of the epigenetic concept is that natural selection does not determine the basic morphological features that are assembled into a new body plan. Those morphological features are developed long before natural selection enters the development sequence, stated as follows:

— with no morphological innovation being involved, the evolution of limb bud shape can be well-accommodated within the neo-Darwinian paradigm. (38)

But the essential evaluation of the epigenetic’s relationship to WEiT’s perception of the creative role that natural selection plays in the development of new body plans is forcefully disputed by Newman et al. as follows:

Neo-Darwiniam mechanisms, in which biological forms typically change in incremental fashion due to genes of “small effect,” may only pertain to systems sufficiently evolved so that numerous gene and gene-gene interactions have come to serve canalizing and fine-tuning functions—. (38) [emphasis supplied]

Skeletal novelties that arise from such a mechanism could remain selectively neutral for long periods of time, since their existence in every generation merely depends on the maintenance of the same biomechanical conditions. But eventually such structures can become subject to selection and, through canalization and stabilizing evolution—, gradually become integrated into the development repertoire—. (38) (emphasis supplied)

The authors further evaluate the actual role of natural selection in the development of novelty body plans as follows:

Natural selection can exploit the variation that results from such environmentally dependent phenotypic plasticity—. But — most relevant to the program of morphological innovation is the potential source of skeletal novelty inherent to a mechanism that has the capacity to form de novo elements. Like the core mechanism, these biomechanical effects can elicit morphological novelty as a “saltatory” byproduct of continuous natural selection. Continuous selection on size, shape, or proportion of body parts, such as the relative size of skeletal elements in the limb. (38) [emphasis supplied]

Post 19: Natural Selection: Alternative Genetics Perspective

2010-03-24T20:32:00.000-07:00

One of the closing statements in Post 18 addressed how WEiT’s perspectives concerning natural selection, meshed with the “conventional wisdom” held by at least a representative body of the biological evolution establishment.

A logical starting point for comparing WEiT’s perspective of natural selection’s role in the evolution of “major forms” is evolutionary biology’s concept of “conserved developmental programs,” also referred to as the “conserved genetic toolkit.”

The “conserved genetic toolkit” is an evolutionary biology concept that provides an “evidence” bridge to evaluate WEiT’s perspective of the role that natural selection played/plays in the development of body plans.

The intent of this post is NOT to examine the plausibility of the toolkit concept, but rather to use pertinent aspects of the “toolkit” concept as a basis for why the toolkit concept demonstrates that WEiT’s perception of natural selection’s role in the development of “major forms,” herein diverse body plans, is not plausible.

WEiT did not include the “genetic toolkit” in its argument for why “it” is true and thus as evidence that the main tenents of Darwin’s hypothesis have been verified.

Since there are no specific “toolkit” concepts in the book to bring under the “microscope” of the genetic toolkit concept, other than WEiT’s perspective that genetic changes involved in “species splitting” are responsible for the development of different “major forms:”

— those differences are based on changes in the DNA which originate as mutations. (page 3) [emphasis supplied]

Thus, this post will address generally recognized concepts whose evolutionary roles bear on the plausibility of WEiT’s perception that natural selection is the generative mechanism responsible for the development of “major forms.”

The intent is treat a brief view of the treated concepts to maintains a semblance of brevity in this post’s main body, where additional citations that seem to be relevant can be accessed by links.

Basic Questions

A rationale for the necessity of the “conserved genetic toolkit” is related to the perspective that natural selection is not an adequate mechanism that has been responsible for the profusion of extinct and extant body plans.

How are we to reconcile the conflicting evolutionary scenarios of relationships among early-branching animals with the genesis and early evolution of the genetic toolkit? Was the genetic toolkit causal in the evolution of animal multicellularity or simply its product? (27) [emphasis supplied]

Basic Concept

The “conserved genetic toolkit” is an assortment of genes and gene related products that are observed to be involved in the patterning of the morphological properties of multicelled animals.

The key feature of the toolkit concept is their complement of molecular features which has remained essentially unchanged since their initial appearance in the fossil record:

—the Metazoa have used a highly conserved set of gene products, the so-called developmental-genetic toolkit to generate diverse body and organ form—.(26) [emphasis supplied]

— the basic toolkit for bilaterian morphogenesis is widely shared across Bilateria and did not develop uniquely within individual clades. (31)

Genetic Basis

Evidence for the conserved perspective is the persistence of molecular elements from the proposed time of evolutionary origin of the toolkit, for example:.

Indeed, the function of Hox proteins — which are found in all higher animals — has remained virtually unchanged through time.—Nevertheless, there are rare examples of Hox proteins that have adopted new functions through evolution. (30) [emphasis supplied]

Among the most highly conserved of the development genes are the Hox genes — a large family of genes best known for their role in controlling the pattern of body development. (30) [emphasis supplied]

Functional Origin

Rationale for the time of origin of the “toolkit” is based on the following:

Assembly of the modern genetic tool kit for development and initial divergence of major animal clads occurred during the Proterozoic Eon. (29) [emphasis supplied]

Comparative studies of metazoan development (“evo-devo”) have established to general satisfaction that the toolkit of development machinery was determined quite early in metazoan evolution, indeed before the origin of the Bilateria. (31) [emphasis supplied]

However, the “action element” in the toolkit is not the genes.

— the morphological transitions that gave rise to the phyla cannot be extrapolated from their living descendants. It will require a far richer Proterozoic and earliest Cambrian fossil record to solve the problem paleontologically. And the keys to the origin of body plans are not likely to be the sort of genetic innovations that occurred in the bilaterian stem lineage;— Rather, the differences in body plans are likely to have arisen at the level of the regulatory networks [GRN’s] that organize pattern formation. (29) [emphasis and bracketed text supplied]

Major Forms

But the most significant argument against WEiT’s perception of “major forms” having developed from small changes in small-step mutations is based on the mechanism of the “toolkit” in functioning of genes.

These observations suggest that bilaterian body plan diversification has occurred primarily through changes in developmental regulatory networks rather than the genes themselves which evolved much earlier. (29) [emphasis supplied]

In the interplay between genetics and physics in the production of organismal form, then, genes ensure the perpetuation of variations on biological themes but they do not define the themes themselves. (28) [emphasis supplied]

— it has been conclusively established that much of the incredible diversity of form among metazoans rests not on entirely new genes, or even novel regulatory and developmental schemes, but on rewiring the relationships among conserved signalling molecules. (31) [emphasis supplied]

The modern descendants of these forms, including the chelicerates, crustacea, myriapods, insects, and onychophora, illustrate all the elements of the body plan diversity apparent in Cambrian assemblages, including the major differences in tagmosis, segment and appendage number, and limb morphology. (29) [emphasis supplied]

Species Splitting

Considering WEiT’s perspective on species splitting as the “event” that set body-plan diversification in motion, the acquisition of major innovations is contrary to the collective perspectives of evolutionary biology that such innovations are developed by splitting and subsequent morphological change.

The three-branched bilaterian tree [not shown herein] provides no extant candidates for the sort of animal that could represent the hypothetical last common ancestor of protosomes and deutersomes, dubbed Urbilateria. (29) [emphasis and bracketed text supplied]

The discontinuity between cnidarian and bilaterian body plans as well as the probable complexity of Urbilateria suggests that the evolution of bilaterian characteristics must have required many innovations, including a third germ-layer, bilateral symmetry, a centralized nerve cord, a through gut, various primitive organs, and the genetic systems to organize and pattern these features. It is not clear to what degree any extant taxon represents an intermediate in the anatomical or genetic evolution of bilaterian organization. (29) [emphasis supplied]

Natural Selection

The “toolkit” has several implications for the plausibility of WEiT’s perspective of the role natural selection plays in the development of extinct and extant “major forms,” (1) the time that natural selection operated; and (2) the magnitude of morphological change in connection with “major forms;” and (3) sequence of morphological change.

Time

Current studies of “evo-devo,” the relationship between developmental programs and patterns of evolution, have demonstrated highly conserved patterns of gene expression and developmental sequencing in the organization of the body plan, the brain, and the eye, quite unlike the cumulative diversification of developmental programs across major taxa that selection or random adaptations would suggest. (32) [emphasis supplied]

Magnitude

—evolutionary theory has traditionally held that very long periods of time were needed for natural selection to generate extreme differences in morphological organization like those seen in animal body plans. In particular, the neo-Darwinian mechanism for such large-scale change was the accumulation, along mulitple evolutionary trajectories, of incremental gene-related (i.e., microevolutionary) departures from a common ancestral morphology. This view was shaken by the recognition over the last quarter century that essentially all modern metazoan body plans burst into the biosphere over a relatively short period of time, geologically speaking, perhaps 20-30 million years during the late pre-Cambrian and early Cambrian periods about 530-570 million years ago. (28) [emphasis supplied]

Sequence

—the first metazoans would, with minimal genetic change, have taken on many forms in variable physical environments. Natural selection could then act on this morphological variation to sharpen the means by which some of the variants were generated, a process that has been termed “stabilizing.” (28) [emphasis supplied]

Rapid morphological evolution is compatible with classic neo-Darwinian evolutionary mechanisms of random genetic change followed by natural selection, whereby existing structures are modified in their size and shape—. Nonetheless, the discovery of the phylum-level diversification (with no evident intermediates) that occurred in the early Cambrian is not anticipated by this theory—.(26) [emphasis supplied]

The fundamental problem in WEiT’s perception that the development of “major forms” is initiated with “species splitting” is: where, in the continuum of gene mutation to completed morphological body plan continuum, does natural selection perform its supposed role of promoting the “fittest major forms?”

This question leads to what evidence has been observed that would supply answers to the following questions.

Do the “fittest mutations” undergo natural selection before the attainment of what can be logically designated a completed body plan,” or does the weeding out of the unfit occur after the development achieves a completed body plan?

If the former, at what stage of the developing body plan of the “fittest” animal does natural selection apply its selection mechanism?

If the latter, after a “species splitting” event, do the resulting “fittest” and “unfit” survive in parallel as developing organisms until both the “most fit” and the “least fit” achieve some taxonomic rank where natural selection comes into play?

Conclusion

Regardless of the “finer details” involved with the genetic toolkit concept, evolutionary biology research scientists have assembled evidence, as very briefly treated in this post, concluding that the essential mechanism(s) that have produced the variety of extinct and extant animal body plans were established without WEiT’s declaration the such developments in the process of species splitting, were due to “changes in DNA which originate as mutations.”

Toolkit Operational Instructions

The field of “epigenetics” (also not treated in WEiT) has developed perspectives concerning where in the body-plan development sequence and under what conditions do events occur that establish the known body plans, both of which are counter to WEiT’s perspectives.

Chapter 5 in Carrol’s book (33) is titled “The Dark Matter of the Genome: Operation Instructions for the Tool Kit” and is an apt statement to introduce the subject of the next post which treats the question of the“mechanism” responsible for exercising/applying the “toolkit’s genetic complement.”

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

21. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

22. Valentine, James W. and David Jablonski. Morphological and developmental macroevolution: a paleontological perspective. Int. J. Dev. Biol. 47, 2003.

23. Valentine, James W. Late Precambrian Bilaterians: Grades and Clades.. Tempo and Mode in Evolution: Genetics and Paleontology 50 Years After Simpson. 1995.

24. 7. Arthur, Wallace. The origin of animal body pl;ans: A study in evolutionary developmental biology. Cambridge University Press. 1997 & 2000.

25. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

26. Newman, Stuart A. and Ramray Bhat. Dynamical patterning modules: s “pattern language” for development and evolution of multicellular form. Int. J. Dev. Biol. 53: 693-705 (2009).

27. Rokas, Antonis. The Origins of Multicellularity and the Early History of the Genetic Toolkit For Animal Development. Annu. Rev. Genet. 2008. 42: 235-51.

28. Newman, Stuart A. The Developmental Genetic Toolkit and the Molecular Homology-Analogy Paradox. Biological Theory. 1 (1) 2006

29. Knoll, Andrew H. and Sean B. Carrol. Early Animal Evolution: Emerging Views From Comparative Biology and Geology. (?????????)

30. Carrol, Sean B., Jennifer Grenier and Scott Weatherbee. From DNA To Diversity: Genetics and the Evolution of Animal Design. Wiley-Blackwell. 2001.

31. Erwin, Douglas H. Disparity: Morphological Pattern And Developmental Context. Palaeontology. Vol. 50, Part 1. 2007.

32. Dyer, Michael A., Rodrigo Martins, Manoel da Silva Filho, Jose Augusto P. C. Muniz,

33. Carrol, Sean B. Endless Forms Most Beautiful : The New Science Of EvoDevo. and The Making Of The Animal Kingdom. W. W. Norton And Company, Inc.

Post 18: Natural Selection-WEiT Perspective

2010-03-03T09:07:00.000-08:00

The intent of this post is to establish WEiT’s overall perspective of natural selection by arranging its numerous references into several “levels” that will serve as a logic sequence for deductively evaluating the plausibility of “levels” 1 and 2 based on the plausibility of the “critical category” that is singly treated in level 3.

The three “levels”into which WEiT’s reference seem to comfortably fit into are:

(1) WEiT’s perception of natural selection’s explanatory requirements;

(2) WEiT’s perception of natural selection’s “status of acceptance” as a biological evolution mechanism;

(3) WEiT's perception of how biological science knows how natural selection is the mechanism responsible for the proliferation of extinct and extant body plans from Darwin’s hypothesized common ancestor.

Explanatory Requirements

As treated in earlier posts, WEiT definitively establishes the scientific requirements that natural selection must satisfy as a mechanism responsible for body plan proliferation from a common ancestor:

The theory of natural selection has a big job–the biggest in biology, Its task is to explain how every adaptation evolved, step by step, from traits that preceded it. This includes not just body form and color, but the molecular features that underlie everything. Selection must explain the evolution of complex physiological features—. (page 119) [emphasis supplied]

The key point in this description lies in WEiT’s perception of natural selection as the causation and adaptation as the effects of the causation, with the changed features ranging from molecular to physiological and morphological.

Three things are involved in creating an adaptation by natural selection. First, the starting population has to be variable.—Second, some proportion of that variation has to come from changes in the forms of genes, that is, the variation has to have some genetic basis (called heritability).—The third and last aspect of natural selection is that the genetic variation must affect an individual’s probability of leaving offspring. (Page 118) [emphasis supplied]

The critical feature in this perspective is that molecular, physiological and morphological features are the “objects” that were changed, not the mechanism(s) that caused the objects to change that then resulted in the adaptation.

The second quote suffers from the same kind of misrepresentation—genes and/or genetic variation are the objects of the change, not the mechanism(s) that caused the genes/genetic variation to change.

Status Of The “Theory”

It is relevant to relate the current status of natural selection’s place, which WEiT refers to as a "theory," in evolutionary thinking, to the original perspective presented by Darwin.”

In the book’s Chapter 5, entitled “The Engine of Evolution,” WEiT states the following as a historical reference to the mechanism’s status in biological science:

In a single chapter, he [Darwin] completely replaced centuries of certainty about divine design with the notion of a mindless, materialistic process — natural selection — that could accomplish the same result. (Page 115) [emphasis and bracketed text supplied]

WEiT brings this level of assurance into the current view with the following:

Now, when we say that “evolution is true,” what we mean is that major tenents of Darwinism have been verified. Organisms evolved, they did so gradually, lineages split into different species from common ancestors, and natural selection is the major engine of adaptation. (Page 223) [emphasis supplied]

—the mechanism for most (but not all) of evolutionary change is natural selection. (page 3) [emphasis supplied]

How The Science “Knows”

WEiT’s treatment of how the science knows that natural selection is a mechanism that has produced body-plan proliferation is, beyond the actual subject matter, a perception framework that is perhaps best illustrated by dividing the “know” references into three levels of “plausibility”: (1) can natural selection be observed? (2); natural selection can’t be observed; and (3) natural selection can be/is observed.”

Which one of these options represents reality is the criterion to judge biological science’s achievement of the foregoing “explanatory requirements.”

“Can Natural Selection Be Observed?”

Sure, selection can change the beaks of birds, —but can it build complexity. What about intricate traits like—exquisite biochemical adaptations like blood clotting, which entails a precise sequence of steps involving many proteins;—. (page 136) [emphasis supplied]

—complex features take a long time to evolve, and most of them did so in the distant past when we weren’t around to see how it happened. So how can we be sure that selection was involved? (Page 136) [emphasis supplied]

“Natural Selection Can’t Be Observed”

—it’s unreasonable to expect to see selection transforming one “type” of plant or animal into another—so-called macroevolution--within a human lifetime. Though macroevolution is occurring today, we simply won’t be around long enough to see it — the issue is not whether macroevolution change happens–we already know from the fossil record that it does – but whether it was caused by natural selection, and whether natural selection can build complex features and organisms. (page 133) [emphasis supplied]

If there is one declaration in the book that established a base for the plausibility of all the other explanations and examples, the foregoing is a leading candidate.

The key combination in the foregoing statement is WEiT’s marrying of “type” with “macroevolution” which is commensurate with “body plans” as recognized in the opening statement in the foregoing section on natural selection’s status in the science.

This recognition by WEiT is arguably the seminal statement against which the claims in the following section must be compared to evaluate their plausibility and thus the plausibility of the book’s entire argument that Darwin’s hypothesis of biological evolution is “true.”

One overriding point is to be stressed in each evaluation is the plausibility of the claims (or more accurately expressed as reality):

The effect (or product) whose mechanism(s) of development is to be observed and thus empirically documented is body-plan diversification.

If the specific reference to “can be/is” is not dynamically connected in a described cause/effect relationship as a mechanism that causes body-plan change, then the reference is only a perceived relationship (i.e., causative mechanism) and is open to alternative perceptions.

We’ll never be able to reconstruct [see]how selection created everything — evolution happened before we were on the scene, and some things will always be unknown. (Page 137) [emphasis and bracketed text supplied]

WEiT’s perception of natural selection’s reality appears to be interpretable in two ways.

Perhaps the most striking demonstration of contrasting explanations of natural selection occurs in the perspective on one hand that natural selection must explain how “every adaptation evolved step by step’ and “we’ll never be able to reconstruct how selection created everything — some things will always be unknown.”

This conflict in the plausibility of WEiT’s explanation of natural selection can be argued to call into doubt the claim that “natural selection is the mechanism of most evolutionary change:”

This observation has further implications for evaluating the plausibility of the “can be/is” references: What observation/evidence is required to specify what adaptations can be classified as the “some things that will always be unknown?”

Do the “some things that will always be unknown” include: some of the molecular properties; or some of the complex physiological properties; or some of the complex body-plan arrangements; or some of the genetic makeup properties; or some of the “codependent parts”; or some of the mutations (but not addressed); all of which are elements in WEiT’s charge that every adaptation that natural selection must explain step-by-step?

If so, how is one to assemble a reasonably descriptive step-by-step sequence of cause and effect relationships, i.e. mechanism(s) and its products — how many unknown mechanism-steps are to be “accepted” before the step-by-step sequence itself is unacceptable, particularly when by definition the importance of the unknowns in the process is unknown?

“Natural Selection Can Be/Is Observed”

WEiT makes a number of positive declarations to be evaluated:

First, natural selection can promote the evolution of complex, interconnected biochemical systems in which all the parts are codependent—. (page 129) [emphasis supplied]

Natural selection remains the only process that can produce adaptation. (Page 13) [emphasis supplied]

—What’s the alternative theory? We know of no other natural process that can build a complex adaptation. (Page 136) [emphasis supplied]

There are many more examples, but they all demonstrate the same thing: we can directly witness [see] natural selection leading to better adaptation. (Page 136) [emphasis and bracketed text supplied]

If we want to see selection in action, then, we should look in species that have short generation times and are adapting to a new environment. (Page 133) [emphasis supplied]

We should be able to see natural selection acting in the wild. (Page 18) [emphasis supplied]

These statements involving “can” and “see” have no bearing for explaining the mechanism(s) that are involved in changing molecular, physiological, or body plan features. What is “seen” is the result or product of the mechanism(s), not the actual mechanism.

Also, the changes that may be observed and documented are not the “major form” changes that are treated in Post 16, as WEiT recognized in the statement “though macroevolution is occurring today, we won’t be around long enough to see it.”

Since the foregoing analysis presents a reasonably valid line of logic, where does it leave the credibility of Darwin’s hypothesis in the following justification of the hypothesis’ credibility:?

Finally, is natural selection sufficient to explain a really complex organ, such as the eye? The “camera” eye of vertebrates (and mollusks like the squid and octopus) was once beloved by creationists. Noting its complex arrangement of the iris, lens, retina, cornea, and so on—all of which must work together to create an image—opponents of natural selection claimed that the eye could not have formed by gradual steps. How could “half an eye” be of any use? Darwin brilliantly addressed, and rebutted, this argument in The Origin. He surveyed existing species to see if one could find functional but less complex eyes that were not only useful but could be strung together into a hypothetical sequence showing how a camera eye might evolve. (Page 141) [emphasis supplied]

This implication of “certainty” from Darwin's act of "seeing" does not seem to carry into the following:

Despite the unknowns, we can make some guesses about how natural selection fashioned modern birds. (Page 46) [emphasis supplied]

To really see the power of selection, we must extrapolate the small changes that selection creates in our lifetime over the millions of years that it has really had to work in nature. (page 143) [emphasis supplied]

It’s not hard to accept the idea that natural selection could cause, say, the evolution of whales from land animals over millions of years, but somehow the idea of selection becomes more compelling when we see the process act before our eyes.—But if we can see selection causing small changes over just a few generations, then perhaps it becomes easier to accept that, over millions of years, similar types of selection could cause the big adaptive changes documented in fossils. (Page 125) [emphasis supplied]

The “bottom line” to consider is: which of the various perceptions treated in this post represents the actual status of the hypothesis as the conventional wisdom of natural selection in evolutionary biology?

In respect to the foregoing examination of WEiT’s perspectives in the three “levels” of natural selection, it seems appropriate to comment that WEiT must include itself in the following observation:

Natural selection is the most misunderstood part of Darwinism. (Page 116) [emphasis supplied]

Post 17: "Major-Form" Change Examples-WEiT Perspective

2010-02-25T08:55:00.000-08:00

The basis for examining WEiT’s body-plan change perspective is a statement called forward from its initial treatment in Post 12 :

A morphological novelty can be defined as “a structure that is neither homologous to any structure in the ancestral species, nor homologous to any other structure of the same organism— This excludes simple continuous variation as a sufficient mechanism for the origination of morphological homologies and hence requires explanations that go beyond the standard Darwinian model, which applies to variation. (15) [emphasis supplied]

In referring to the foregoing definition of a morphological novelty, Muller and Wagner provide the following clarification examples:

In accordance with our considerations above, excludes simple quantitative variation or negative traits. In addition, it allows a distinction between meristic variation, e.g. additional bristles or fin rays, and novelties like the marsupial bone or the panda’s thumb. Additional bristles are both homologous to the bristles already present in the source population and homonomous to all other bristles on the same fly. (17) [emphasis supplied]

In Chapter 2, under the section “Fossilized Evolution and Speciation,” WEiT provides the following examples of morphological changes which are at odds with the foregoing Muller and Muller/Wagner perspective of morphological novelties as essential features that must be considered in determining whether a morphological change represents a different “major form” (in WEiT’s terminology), or new body plan as defined in this blog.

Number of chambers in a marine formainiferan (page 29).

Width of cylindrical base in a radiolarian (page 30).

Number of pygidial ribs in trilobites (page 31).

Size and shape of plankton (width of fourth segment) (page 32).

As a specific example of WEiT’s departure from the novelty concept of Muller and Wagner, in WEiT’s Figure 6 concerning trilobites, the caption contains the statement “displayed a net increase in rib numbers” which is comparable to the morphological features that do not represent body-plan-level changes, i. e., additional bristles or fin rays.

The point to be emphasized is not so much the listing of these particular examples, but rather that they are emblematic of most of the speciation-small-step examples in the book—they represent “simple continuous variations” in body forms and have not been shown to provide plausible evidence for Muller’s second category of novelties, under the definition of Muller/Wagner, that occurred after the development of phylum-level body plans.

In summary, WEiT’s morphological change examples do not contribute to the “trueness” of evolution in relation to Darwin’s hypothesis.

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

19. Davidson, Eric H. and Douglas H. Erwin. Gene Regulatory Networks and the Evolution of Animal Body Plans. Science. Vol. 311, February 10, 2006.

20. Coyne, Jerry A. Comment on “Gene Regulatory Networks and the Evolution of Animal Body Plans. Science Magazine. 21 February 2006.

Post 16: "Major Form" Development-Alternative Perspective

2010-02-05T19:23:00.000-08:00

WEiT’s brief treatment of the Cambrian “major form” events is all the more puzzling since therein lies what a reasonable representation of evolutionary biology considers to be a pivotal morphological form developmental period.

For the purposes of analyzing WEiT’s perspectives on morphological development, this post will treat the development of morphological forms as separate events: the pre-Cambrian, Cambrian and post Cambrian events as the criteria to judge the book’s perspective concerning “major forms” development.

If the previous posts failed to develop a convincing argument challenging the plausibility of “Why Evolution is True” in terms of Darwin’s major tenent of gradualism, the book’s failure to address the concept of body-plan origins provides the culminating argument.

Pre-Cambrian Morphological Form Considerations

Central for critiquing is Coyne’s (and WEiT’s) emphasis on “speciation events” and particularly the perspective that speciation events before or during the Cambrian (as treated in Post 15) were precursors to the Cambrian faunal developments.

The morphological developmental events leading to the “explosion” of Cambrian body plans, i.e., body plans, are interpreted (by a number of “credentialed” biologists) differently from those expressed directly by Coyne and indirectly in the book.

Of the numerous sources whose expertise could be cited that are at variance with Coyne and WEiT, several of the most explicit interpretations are as follows:

The fossil record of the last 3.5 billion years thus shows not a gradual accumulation of biological form, but a relatively abrupt transition from body plans of single cells to those of a rich diversity of animal phyla. (21) [emphasis supplied]

Although those of us who study evolution can infer a great deal about the body plans of the first animals that left traces on the sea floor, we obviously do not have their actual genes and cannot evaluate their relationship from molecular evidence. We are sure that they were moderately complex forms with three tissue layers, but we have no evidence of their relationship to the many living phyla that came afterwards.(18) [emphasis supplied]

Unfortunately there is thus no direct fossil evidence of the morphological features of the earliest members of the bilaterian clades, the bodyplans of the phyla come to us ready-made. (22) [emphasis supplied] [see complete paragraph citation] [see complete citation]

By the time of the Cambrian explosion, some metazoan bodies were as complex as primitive arthropods and other higher invertebrates. This rise in complexity is obscured in the fossil record. (23) [emphasis supplied] [see complete citation]

All of the basic architectures of animals were apparently established by the close of the Cambrian explosion,--- (21) [emphasis supplied] [see complete citation]

The significance of these foregoing perceptions concerning the rise of the Cambrian fauna lies in their explicit interpretation of evidence, and not in personal beliefs or assumptions.

Thus, as treated in Post 15, any reliance by WEiT on pre-Cambrian trait development to bolster its perspective of trait development in a species development context that led to the Cambrian body-plan development has no evidential basis.

Cambrian Morphological Form Considerations,

Arthur (24) contains a table (Table 2-2. Relationship between body plans and taxonomic levels (Parentheses indicate the less clear-cut cases.)) that lists the relationships. (emphasis supplied)

Taxonomic Characterized by
Level a body plan?
Species No
Genus No
Family (No)
Order (Yes)
Class Yes
Phylum Yes
Superphyletic group (No)

Arthur offers the following text.

At the upper levels of the taxonomic hierarchy, phyla- or class-level clades are characterized by their possession of particular assemblages of homologous architectural and structural features...it is to such assemblages that the term Bauplan is applied. (24) [emphasis supplied]

One of Kemp’s papers (8) opens with an introduction containing the following statement that specifically recognizes body plans and their association as major transitions.

For all its fundamental biological interest, the study of evolutionary processes leading to major transitions-– the origin of basic body plans and new higher taxa—is remarkably neglected in the evolutionary literature. [emphasis supplied]

Post-Cambrian Morphological Form Considerations

Two levels of evaluation are relevant for evaluating WEiT’s contention that these development sequences support its argument of “Why Evolution is True”, the first based on general fossil evidence and the second based on specific morphological characteristics of the fossil body forms.

Magnitudes Of Morphological Change

First, concerning the general perspective, evolutionary biology has, to a significant extent, arrived at one overriding conclusion concerning morphological development in terms of body form change since the Cambrian.

---subsequent evolutionary changes, even those that allowed animals to move out of the sea onto land, involved only modification of those basic body plans—. (25) [emphasis supplied] [see complete citation]

The pattern of divergence among the phyla does not solve the larger problem, for the branching sequence tells biologists too little about when the body plans themselves originated.(25) [emphasis supplied] [see complete citation]

All minor clades are modifications of those major body plans,-- (16) [emphasis supplied] [see complete citation]

Transitional “Pairs” As Evidence For Sequential Changes

The fundamental question to be answered in this section has implications for WEiT’s entire perception of the pre-existing trait/new trait transitional change and resulting “species splitting,” as a causative process for major forms: do the transitional-form “Pairs” cited by WEiT qualify as evidence concerning the origins and implied sequences of morphological changes in extinct and extant diverse body plans?

WEiT’s principal perspective of animal-form development can be summarized in the book’s treatment of the transitions between the following “ancestor-descendant” pairs brought foreward from Post 15:

While we may speculate about the details, the existence of transitional fossils—and the evolution of birds from reptiles — is fact. ”[page 47]

One of the greatest fulfilled predictions of evolutionary biology is the discovery, in 2005, of a transitional form between fish and amphibians. [page 35]

There is the transition between reptiles and mammals. (Page 52)

Other references involving “transitional forms include the following:

Fish and amphibians (pages 35-38)
Amphibians and reptiles (page 28)
Reptiles and mammals (pages 21, 25, 52, 53, 71, 79)
Dinosaurs and birds (pages 39-47, 53, 66, 138, 195)
Land mammals and whales (pages 26, 47-52, 53)

But what do these “transition pairs” indicate concerning sequential changes of major forms?

Do these transitional pairs adequately represent the continuum of development events wherein new morphological forms appear in the fossil record?

Specifically, is there documented evidence that pre-existing traits, either individually or collectively, cannot be evoked in appearance of new morphological forms?

Although WEiT’s “transition pairs” do not blend into an orderly sequence, their “position” in the overall development of animal forms can be placed in the following Figure 1, assembled primarily from pertinent “units” in the web page Palaeos.

FIGURE 1

Caption For Figure 1

(1)—it has been necessary to change the very backbone of the vertebrate cladogram—. The origin of chordates now seems to date back to Pre-Cambrian times, perhaps 600My. (UNIT 20: CRANIATA]
(2) [concerning Craniata] Here we enter a strange and poorly known area of phylospace, one in which both timing and phylogeny are poorly understood. Somewhere between 750 and 500 million years ago, a new line of chordates evolved. (UNIT 20: CRANIATA)
(3) Few scientists are courageous enough to speculate in public about the origin of thelodonts. (UNIT 50: THELODONTI)
(4) The origins of the teleostomes are obscure, but their first known fossils are Acanthodians (”spiny sharks”) from the Late Ordovician Period. (From Wikipedia-TELEOSTOMI)
(5) Oddly enough, we have almost no idea what this primordial osteichthian was like — (UNIT 90: TELEOSTOMI)
(6) ---tetrapods originated somewhere within the fleshy-finned or lobed-finned fishes (sarcopterygii), although total agreement does not exist on which sarcopterygian group is ancestral to them. (UNIT 50: THELODONTI)
(7) Although there is a suite of characters unique to most known tetrapods,— not all these characters evolved at once, and the sequence of their evolution is unknown in many cases. This is to be expected if tetrapods evolved by a gradual process, which is what most scientists believed happened. Furthermore, the same must be true of limbs and digits — they evolved gradually by stages. Thus, difficult questions arise: when can an appendage really be called a limb, and so at what point does a tetrapod really become a tetrapod? In fact, if evolution is gradual, then there is no precise point in the continuum at which a line can be drawn to distinguish indisputably a limb from a fin, or a tetrapod from a fish. (26)
(8) If all of the stem tetrapods were aquatic, then how on earth (so to speak) did the transition to terrestrial life take place? If every one from Acanthostega through the colosteids, baphetids, Greererpeton, etc. was aquatic, then we have no reason to suppose that the early reptilomorphs and temnospondyls were any different. These animals are all designed along the same general plan—. The answer seems to lie in a developmental anomaly. (UNIT 170: LEPOSPONDYLI)
(9) Recognizable basal-group Amphibia are representative of the labyrinthodonts, which are comprised of the temnospondyls— and similarly primitive anthracosaurs who were the relatives and ancestors of the Amniota. Depending on whichever authorities one follows modern amphibians (frogs, salamanders and caecilians) are derived from one or the other (or possibly both, although this is now a minority position) of these two groups. (UNIT 150: TETRAPODA)
(10) Amphibians and amniotes must have had a common ancestor at some stage among the early tetrapods that was related equally to both but strictly belonged to neither.—Although this common ancestor will probably always remain hypothetical, it would lie at the node where the lineages of amphibians and amniotes join. (26)
(11) Thus we are looking at an evolutionary succession or continuum, at some point of time along which there was an evolutionary breakthrough represented by the amniote egg. How this happened is still a matter of some speculation. (UNIT 190: REPTILOMORPHA)
(12) The real turn to terrestriality begins here, with the Reptilomorpha.—Although the first amniote reptile probably appeared as early as the Mississippian period—. (UNIT 190: REPTILOMORPHA)
(13) —the comparison of basal therapsids to derived therians leads nowhere. It only tempts us to invoke “trends” under the metaphysical influence of which, like a pantheon of warring godlets, evolution is supposed to take place. (UNIT 400: THERAPSIDA)
(14) Some time in the Middle Triassic, the mammaliformes derived from near one of two branches of the cynodont family: either the tritylodonts or the trithelodonts. (UNIT 420: MAMMALIFORMES)

When WEiT’s reptile to mammal transition, as a representation of WEiT’s perspective, is compared with parallel organisms as expressed in their technical terminology, three critical features are readily apparent.

First, there are significant stages in the development sequence where an animal form occurs in the fossil record that cannot be plausibly linked to a “pre-existing” animal form, and specifically the “appeared” animal form with its multitude of specific traits cannot be claimed to have developed from a documented “pre-existing” trait.

Second, even if the example could be shown to represent a plausible example of transitional forms as evidence, the reptile to mammal example only represents a section of the entire development sequence and cannot be cited as evidence in support of “descent from a common ancestor” since the example starts with a completed body plan whose implied sequence origin is fraught with the same sort of discontinuities as in the sequence.

Third, and directly applicable to WEiT’s “pre-existing trait” to “new trait” change achieved via small steps, based on the discontinuities in both WEiT’s reptile to mammal example and in the overall sequence in Figure 1, the concept cannot be invoked as a mechanism in the occurrence in a fossil history within which there are numerous new “major forms” occurrences of animals whose form cannot be linked to an immediate precursor.

The foregoing three observations lead to the seminal question concerning WEiT's principle perspective of "species splitting" as the mechanism/process/event responsible for morphological diversification.

If the discontinuities that repeatedly occur before the appearance of a "major form," as illustrated in Figure 1, are where the mechanism causing morphological diversification occur, then WEiT's "species splitting" only expresses results in minor morphological changes that cannot be perceived as the causation of "major form" development.

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

21. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

22. Valentine, James W. and David Jablonski. Morphological and developmental macroevolution: a paleontological perspective. Int. J. Dev. Biol. 47, 2003.

23. Valentine, James W. Late Precambrian Bilaterians: Grades and Clades.. Tempo and Mode in Evolution: Genetics and Paleontology 50 Years After Simpson. 1995.

24. 7. Arthur, Wallace. The origin of animal body pl;ans: A study in evolutionary developmental biology. Cambridge University Press. 1997 & 2000.

25. Erwin, Douglas, James Valentine, and David Jablonski. The Origin of Animal Body Plans. America Scientist. March-April, 1997.

26. Clack, J. A. Gaining Ground: The Origin and Evolution of Trtrapods. Indiana University Press, Bloomington, 2002.

Post 15: "Major Form" Development-WEiT Perspective

2010-02-05T18:29:00.000-08:00

Other than recognizing that “major forms” (whose morphological features were not defined) were involved in the development of animals, WEiT gives scant attention to the concept of body plans or their inevitable association with Cambrian events.

The Cambrian event is mentioned by name only once:

What caused the Cambrian “explosion” of life, in which many new types of animals appeared within only a few million years?

WEiT does not present a discussion of “what” or any other specific analysis of the event, and indirectly gives rather short attention to body-plan development with the book’s general perspective summarized as follows:

The first organisms, simple photosynthetic bacteria, appear in sediments about 3.5 billion years old–after which we see the first simple “eukaryotes—then— simple but multicelled organisms arise—these groups diversify–with tetrapods— later we find the first true amphibians—reptiles come along.—The first mammals show up—birds show up—After the earliest mammals appear, they—become ever more diverse–the fossils increasingly come to resemble living species. (page 28) [emphasis supplied]

The key perspective in the foregoing concerns the sequence of morphological development, i.e., in jumping from simple multicelled organisms to tetrapods (the first appearance of major biological events (the body plans of tetrapods and similarly animals with equivalent morphological complexity)), the causative “event” (the Cambrian radiation) was not included in the development sequence.

However, Coyne’s treatment of the body-plan events associated with the Cambrian is apparently influenced by the response to a paper published by Davidson and Erwin (19) in which Coyne states the following:

Their underlying assumption [of Davidson and Erwin] is that evolution during the Cambrian involved phylum-level changes in body plans, with all phyla emerging suddenly and no new phyla or body plans arising since then.---It seems more reasonable to assume that the speciation events that occurred during the Cambrian and thereafter did not produce new phyla but merely new species differing from each other and their ancestor in minor ways. Only over long periods of time, during which many species became extinct, did the ancestor of the distinct groups we call “phyla” acquire the traits that made them so distinct. It is hard to believe that a given speciation event could produce a taxon having a radically different group of traits—i.e., a new phylum arising in one step.(20) [emphasis and bracketed text supplied]

The treatment of body-plan origins in Post 16 provides a perspective that is significantly out of agreement with the WEiT and raises the possibility that the book presents a personal viewpoint of “Why Evolution is True” rather than a reasonably balanced perspective that is readily evident in evolutionary biology literature.

Literature Cited

1. Muller, Gerd B. and Newman, Stuart A. Origination of Organismal Form: The Forgotten Cause in Evolutionary Theory. MIT Press, Boston 2003.

2. Meyers, PZ. Pharyngula. December 21, 2007.

3. Lamb, Trevor D., Shaun P. Collins, And Edward N. Pugh, Jr. Evolution Of The Vertebrate Eye: Opsins, Photoreceptors, Retina and Eye Cup. Nature Reviews Neuroscience 8, 960-976. December 2007.

4. Gregory, T. Ryan. The Evolution of Complex Organs. Evo. Edu. Outreach. October 2008.

5. Oakley, Todd H. and M. Sabrina Pankey. Opening the “Black Box”: The Genetic and Biochemical Basis of Eye Evolution. Evo. Edu. Outreach. Oct. 2008.

6. Salvini-Plawen L. V., and E Mayr. On the evolution of photoreceptors and eyes: Evolutionary Biology, v. 10. New York: Plenum Press; 1977.

7. Nilsson, D. E. and S. Pelger. A pessimistic estimate of the time required for the eye to evolve. Philos Trans R. Soc Lond. B. 1994; 256: 53-8.

8. Kemp, T. S. The concept of correlated progression as the basis of a model for the evolutionary origin of major new taxa. Proc. R. Soc. B (2007) 274, 1667-1673.

9. Kemp, T. S. The origin of mammalian endothermy: a paradigm for the evolution of complex biological structure. Zoological Journal Of The Linnean Society, 2006, 147, 473-488.

10. Kemp, T. S. The origin of higher taxa: macroevolutionary processes, and the case of the mammalia. Acta Zoologica (Stockholm) 88:3-22 )January 2007).

11. Budd, Graham E. On the origin and evolution of major morphological characters. Biol. Rev. Camb. Philos. Soc., 81, 609-28 (2006).

12. Hunter, Cornelius. Survey of failed evolutionary predictions. http://www. Darwin’s Predictions.com

13. Muller, Gerd B. Developmental Mechanisms at the Origin of Morphological Novelty: A Side-Effect Hypothesis. Evolutionary Innovations. M.H. Nitecki. The University of Chicago Press. 1990.

14. Muller, Gerd B. and Newman, Stuart A. The Innovation Triad: An EvoDevo Agenda. Jour. Exp. Zoo., 304B:487-503 (2005).

15. Muller, Gerd B. Novelty and Key Innovations. In: Pagel, Mark. Encyclopedia of Evolution.
Volume 2. Oxford University Press.2002.

16. Muller, Gerd B. Homology: The Evolution of Morphological Organization. In; Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. A Bradford Book. The MIT press.

17. Muller, Gerd B. and Gunter P Wagner. Novelty In Evolution: Restructuring The Concept. Annu. Rev. Ecol. Syst. 1991.

18. Grasse, Pierre P. Evolution Of Living Organisms. Academic Press. 1977.

19. Davidson, Eric H. and Douglas H. Erwin. Gene Regulatory Networks and the Evolution of Animal Body Plans. Science. Vol. 311, February 10, 2006.

20. Coyne, Jerry A. Comment on “Gene Regulatory Networks and the Evolution of Animal Body Plans. Science Magazine. 21 February 2006.