Stephen C. Meyer Article: The Origin of Biological Information and the Higher Taxonomic Categories

Proceedings of the Biological Society of Washington ^ | January 26, 2005 | Stephen C. Meyer

[DannyTN]

On August 4th, 2004 an extensive review essay by Dr. Stephen C. Meyer, Director of Discovery Institute's Center for Science & Culture appeared in the Proceedings of the Biological Society of Washington (volume 117, no. 2, pp. 213-239). The Proceedings is a peer-reviewed biology journal published at the National Museum of Natural History at the Smithsonian Institution in Washington D.C.

In the article, entitled “The Origin of Biological Information and the Higher Taxonomic Categories”, Dr. Meyer argues that no current materialistic theory of evolution can account for the origin of the information necessary to build novel animal forms. He proposes intelligent design as an alternative explanation for the origin of biological information and the higher taxa.

Due to an unusual number of inquiries about the article, Dr. Meyer, the copyright holder, has decided to make the article available now in HTML format on this website. (Off prints are also available from Discovery Institute by writing to Keith Pennock at Kpennock@discovery.org. Please provide your mailing address and we will dispatch a copy).

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PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON
117(2):213-239. 2004

The origin of biological information and the higher taxonomic categories
Stephen C. Meyer

Introduction

In a recent volume of the Vienna Series in a Theoretical Biology (2003), Gerd B. Muller and Stuart Newman argue that what they call the “origination of organismal form” remains an unsolved problem. In making this claim, Muller and Newman (2003:3-10) distinguish two distinct issues, namely, (1) the causes of form generation in the individual organism during embryological development and (2) the causes responsible for the production of novel organismal forms in the first place during the history of life. To distinguish the latter case (phylogeny) from the former (ontogeny), Muller and Newman use the term “origination” to designate the causal processes by which biological form first arose during the evolution of life. They insist that “the molecular mechanisms that bring about biological form in modern day embryos should not be confused” with the causes responsible for the origin (or “origination”) of novel biological forms during the history of life (p.3). They further argue that we know more about the causes of ontogenesis, due to advances in molecular biology, molecular genetics and developmental biology, than we do about the causes of phylogenesis--the ultimate origination of new biological forms during the remote past.

In making this claim, Muller and Newman are careful to affirm that evolutionary biology has succeeded in explaining how preexisting forms diversify under the twin influences of natural selection and variation of genetic traits. Sophisticated mathematically-based models of population genetics have proven adequate for mapping and understanding quantitative variability and populational changes in organisms. Yet Muller and Newman insist that population genetics, and thus evolutionary biology, has not identified a specifically causal explanation for the origin of true morphological novelty during the history of life. Central to their concern is what they see as the inadequacy of the variation of genetic traits as a source of new form and structure. They note, following Darwin himself, that the sources of new form and structure must precede the action of natural selection (2003:3)--that selection must act on what already exists. Yet, in their view, the “genocentricity” and “incrementalism” of the neo-Darwinian mechanism has meant that an adequate source of new form and structure has yet to be identified by theoretical biologists. Instead, Muller and Newman see the need to identify epigenetic sources of morphological innovation during the evolution of life. In the meantime, however, they insist neo-Darwinism lacks any “theory of the generative” (p. 7).

As it happens, Muller and Newman are not alone in this judgment. In the last decade or so a host of scientific essays and books have questioned the efficacy of selection and mutation as a mechanism for generating morphological novelty, as even a brief literature survey will establish. Thomson (1992:107) expressed doubt that large-scale morphological changes could accumulate via minor phenotypic changes at the population genetic level. Miklos (1993:29) argued that neo-Darwinism fails to provide a mechanism that can produce large-scale innovations in form and complexity. Gilbert et al. (1996) attempted to develop a new theory of evolutionary mechanisms to supplement classical neo-Darwinism, which, they argued, could not adequately explain macroevolution. As they put it in a memorable summary of the situation: “starting in the 1970s, many biologists began questioning its (neo-Darwinism's) adequacy in explaining evolution. Genetics might be adequate for explaining microevolution, but microevolutionary changes in gene frequency were not seen as able to turn a reptile into a mammal or to convert a fish into an amphibian. Microevolution looks at adaptations that concern the survival of the fittest, not the arrival of the fittest. As Goodwin (1995) points out, 'the origin of species--Darwin's problem--remains unsolved'“ (p. 361). Though Gilbert et al. (1996) attempted to solve the problem of the origin of form by proposing a greater role for developmental genetics within an otherwise neo-Darwinian framework,¹ numerous recent authors have continued to raise questions about the adequacy of that framework itself or about the problem of the origination of form generally (Webster & Goodwin 1996; Shubin & Marshall 2000; Erwin 2000; Conway Morris 2000, 2003b; Carroll 2000; Wagner 2001; Becker & Lonnig 2001; Stadler et al. 2001; Lonnig & Saedler 2002; Wagner & Stadler 2003; Valentine 2004:189-194).

What lies behind this skepticism? Is it warranted? Is a new and specifically causal theory needed to explain the origination of biological form?

This review will address these questions. It will do so by analyzing the problem of the origination of organismal form (and the corresponding emergence of higher taxa) from a particular theoretical standpoint. Specifically, it will treat the problem of the origination of the higher taxonomic groups as a manifestation of a deeper problem, namely, the problem of the origin of the information (whether genetic or epigenetic) that, as it will be argued, is necessary to generate morphological novelty.

In order to perform this analysis, and to make it relevant and tractable to systematists and paleontologists, this paper will examine a paradigmatic example of the origin of biological form and information during the history of life: the Cambrian explosion. During the Cambrian, many novel animal forms and body plans (representing new phyla, subphyla and classes) arose in a geologically brief period of time. The following information-based analysis of the Cambrian explosion will support the claim of recent authors such as Muller and Newman that the mechanism of selection and genetic mutation does not constitute an adequate causal explanation of the origination of biological form in the higher taxonomic groups. It will also suggest the need to explore other possible causal factors for the origin of form and information during the evolution of life and will examine some other possibilities that have been proposed.

The Cambrian Explosion

The “Cambrian explosion” refers to the geologically sudden appearance of many new animal body plans about 530 million years ago. At this time, at least nineteen, and perhaps as many as thirty-five phyla of forty total (Meyer et al. 2003), made their first appearance on earth within a narrow five- to ten-million-year window of geologic time (Bowring et al. 1993, 1998a:1, 1998b:40; Kerr 1993; Monastersky 1993; Aris-Brosou & Yang 2003). Many new subphyla, between 32 and 48 of 56 total (Meyer et al. 2003), and classes of animals also arose at this time with representatives of these new higher taxa manifesting significant morphological innovations. The Cambrian explosion thus marked a major episode of morphogenesis in which many new and disparate organismal forms arose in a geologically brief period of time.

To say that the fauna of the Cambrian period appeared in a geologically sudden manner also implies the absence of clear transitional intermediate forms connecting Cambrian animals with simpler pre-Cambrian forms. And, indeed, in almost all cases, the Cambrian animals have no clear morphological antecedents in earlier Vendian or Precambrian fauna (Miklos 1993, Erwin et al. 1997:132, Steiner & Reitner 2001, Conway Morris 2003b:510, Valentine et al. 2003:519-520). Further, several recent discoveries and analyses suggest that these morphological gaps may not be merely an artifact of incomplete sampling of the fossil record (Foote 1997, Foote et al. 1999, Benton & Ayala 2003, Meyer et al. 2003), suggesting that the fossil record is at least approximately reliable (Conway Morris 2003b:505).

As a result, debate now exists about the extent to which this pattern of evidence comports with a strictly monophyletic view of evolution (Conway Morris 1998a, 2003a, 2003b:510; Willmer 1990, 2003). Further, among those who accept a monophyletic view of the history of life, debate exists about whether to privilege fossil or molecular data and analyses. Those who think the fossil data provide a more reliable picture of the origin of the Metazoan tend to think these animals arose relatively quickly--that the Cambrian explosion had a “short fuse.” (Conway Morris 2003b:505-506, Valentine & Jablonski 2003). Some (Wray et al. 1996), but not all (Ayala et al. 1998), who think that molecular phylogenies establish reliable divergence times from pre-Cambrian ancestors think that the Cambrian animals evolved over a very long period of time--that the Cambrian explosion had a “long fuse.” This review will not address these questions of historical pattern. Instead, it will analyze whether the neo-Darwinian process of mutation and selection, or other processes of evolutionary change, can generate the form and information necessary to produce the animals that arise in the Cambrian. This analysis will, for the most part, ² therefore, not depend upon assumptions of either a long or short fuse for the Cambrian explosion, or upon a monophyletic or polyphyletic view of the early history of life.

Defining Biological Form and Information

Form, like life itself, is easy to recognize but often hard to define precisely. Yet, a reasonable working definition of form will suffice for our present purposes. Form can be defined as the four-dimensional topological relations of anatomical parts. This means that one can understand form as a unified arrangement of body parts or material components in a distinct shape or pattern (topology)--one that exists in three spatial dimensions and which arises in time during ontogeny.

Insofar as any particular biological form constitutes something like a distinct arrangement of constituent body parts, form can be seen as arising from constraints that limit the possible arrangements of matter. Specifically, organismal form arises (both in phylogeny and ontogeny) as possible arrangements of material parts are constrained to establish a specific or particular arrangement with an identifiable three dimensional topography--one that we would recognize as a particular protein, cell type, organ, body plan or organism. A particular “form,” therefore, represents a highly specific and constrained arrangement of material components (among a much larger set of possible arrangements).

Understanding form in this way suggests a connection to the notion of information in its most theoretically general sense. When Shannon (1948) first developed a mathematical theory of information he equated the amount of information transmitted with the amount of uncertainty reduced or eliminated in a series of symbols or characters. Information, in Shannon's theory, is thus imparted as some options are excluded and others are actualized. The greater the number of options excluded, the greater the amount of information conveyed. Further, constraining a set of possible material arrangements by whatever process or means involves excluding some options and actualizing others. Thus, to constrain a set of possible material states is to generate information in Shannon's sense. It follows that the constraints that produce biological form also imparted information. Or conversely, one might say that producing organismal form by definition requires the generation of information.

In classical Shannon information theory, the amount of information in a system is also inversely related to the probability of the arrangement of constituents in a system or the characters along a communication channel (Shannon 1948). The more improbable (or complex) the arrangement, the more Shannon information, or information-carrying capacity, a string or system possesses.

Since the 1960s, mathematical biologists have realized that Shannon's theory could be applied to the analysis of DNA and proteins to measure the information-carrying capacity of these macromolecules. Since DNA contains the assembly instructions for building proteins, the information-processing system in the cell represents a kind of communication channel (Yockey 1992:110). Further, DNA conveys information via specifically arranged sequences of nucleotide bases. Since each of the four bases has a roughly equal chance of occurring at each site along the spine of the DNA molecule, biologists can calculate the probability, and thus the information-carrying capacity, of any particular sequence n bases long.

The ease with which information theory applies to molecular biology has created confusion about the type of information that DNA and proteins possess. Sequences of nucleotide bases in DNA, or amino acids in a protein, are highly improbable and thus have large information-carrying capacities. But, like meaningful sentences or lines of computer code, genes and proteins are also specified with respect to function. Just as the meaning of a sentence depends upon the specific arrangement of the letters in a sentence, so too does the function of a gene sequence depend upon the specific arrangement of the nucleotide bases in a gene. Thus, molecular biologists beginning with Crick equated information not only with complexity but also with “specificity,” where “specificity” or “specified” has meant “necessary to function” (Crick 1958:144, 153; Sarkar, 1996:191).³ Molecular biologists such as Monod and Crick understood biological information--the information stored in DNA and proteins--as something more than mere complexity (or improbability). Their notion of information associated both biochemical contingency and combinatorial complexity with DNA sequences (allowing DNA's carrying capacity to be calculated), but it also affirmed that sequences of nucleotides and amino acids in functioning macromolecules possessed a high degree of specificity relative to the maintenance of cellular function.

The ease with which information theory applies to molecular biology has also created confusion about the location of information in organisms. Perhaps because the information carrying capacity of the gene could be so easily measured, it has been easy to treat DNA, RNA and proteins as the sole repositories of biological information. Neo-Darwinists in particular have assumed that the origination of biological form could be explained by recourse to processes of genetic variation and mutation alone (Levinton 1988:485). Yet if one understands organismal form as resulting from constraints on the possible arrangements of matter at many levels in the biological hierarchy--from genes and proteins to cell types and tissues to organs and body plans--then clearly biological organisms exhibit many levels of information-rich structure.

Thus, we can pose a question, not only about the origin of genetic information, but also about the origin of the information necessary to generate form and structure at levels higher than that present in individual proteins. We must also ask about the origin of the “specified complexity,” as opposed to mere complexity, that characterizes the new genes, proteins, cell types and body plans that arose in the Cambrian explosion. Dembski (2002) has used the term “complex specified information” (CSI) as a synonym for “specified complexity” to help distinguish functional biological information from mere Shannon information--that is, specified complexity from mere complexity. This review will use this term as well.

The Cambrian Information Explosion

The Cambrian explosion represents a remarkable jump in the specified complexity or “complex specified information” (CSI) of the biological world. For over three billions years, the biological realm included little more than bacteria and algae (Brocks et al. 1999). Then, beginning about 570-565 million years ago (mya), the first complex multicellular organisms appeared in the rock strata, including sponges, cnidarians, and the peculiar Ediacaran biota (Grotzinger et al. 1995). Forty million years later, the Cambrian explosion occurred (Bowring et al. 1993). The emergence of the Ediacaran biota (570 mya), and then to a much greater extent the Cambrian explosion (530 mya), represented steep climbs up the biological complexity gradient.

One way to estimate the amount of new CSI that appeared with the Cambrian animals is to count the number of new cell types that emerged with them (Valentine 1995:91-93). Studies of modern animals suggest that the sponges that appeared in the late Precambrian, for example, would have required five cell types, whereas the more complex animals that appeared in the Cambrian (e.g., arthropods) would have required fifty or more cell types. Functionally more complex animals require more cell types to perform their more diverse functions. New cell types require many new and specialized proteins. New proteins, in turn, require new genetic information. Thus an increase in the number of cell types implies (at a minimum) a considerable increase in the amount of specified genetic information. Molecular biologists have recently estimated that a minimally complex single-celled organism would require between 318 and 562 kilobase pairs of DNA to produce the proteins necessary to maintain life (Koonin 2000). More complex single cells might require upward of a million base pairs. Yet to build the proteins necessary to sustain a complex arthropod such as a trilobite would require orders of magnitude more coding instructions. The genome size of a modern arthropod, the fruitfly Drosophila melanogaster, is approximately 180 million base pairs (Gerhart & Kirschner 1997:121, Adams et al. 2000). Transitions from a single cell to colonies of cells to complex animals represent significant (and, in principle, measurable) increases in CSI.

Building a new animal from a single-celled organism requires a vast amount of new genetic information. It also requires a way of arranging gene products--proteins--into higher levels of organization. New proteins are required to service new cell types. But new proteins must be organized into new systems within the cell; new cell types must be organized into new tissues, organs, and body parts. These, in turn, must be organized to form body plans. New animals, therefore, embody hierarchically organized systems of lower-level parts within a functional whole. Such hierarchical organization itself represents a type of information, since body plans comprise both highly improbable and functionally specified arrangements of lower-level parts. The specified complexity of new body plans requires explanation in any account of the Cambrian explosion.

Can neo-Darwinism explain the discontinuous increase in CSI that appears in the Cambrian explosion--either in the form of new genetic information or in the form of hierarchically organized systems of parts? We will now examine the two parts of this question.

Novel Genes and Proteins

Many scientists and mathematicians have questioned the ability of mutation and selection to generate information in the form of novel genes and proteins. Such skepticism often derives from consideration of the extreme improbability (and specificity) of functional genes and proteins.

A typical gene contains over one thousand precisely arranged bases. For any specific arrangement of four nucleotide bases of length n, there is a corresponding number of possible arrangements of bases, 4ⁿ. For any protein, there are 20ⁿ possible arrangements of protein-forming amino acids. A gene 999 bases in length represents one of 4⁹⁹⁹ possible nucleotide sequences; a protein of 333 amino acids is one of 20³³³ possibilities.

Since the 1960s, some biologists have thought functional proteins to be rare among the set of possible amino acid sequences. Some have used an analogy with human language to illustrate why this should be the case. Denton (1986, 309-311), for example, has shown that meaningful words and sentences are extremely rare among the set of possible combinations of English letters, especially as sequence length grows. (The ratio of meaningful 12-letter words to 12-letter sequences is 1/10¹⁴, the ratio of 100-letter sentences to possible 100-letter strings is 1/10100.) Further, Denton shows that most meaningful sentences are highly isolated from one another in the space of possible combinations, so that random substitutions of letters will, after a very few changes, inevitably degrade meaning. Apart from a few closely clustered sentences accessible by random substitution, the overwhelming majority of meaningful sentences lie, probabilistically speaking, beyond the reach of random search.

Denton (1986:301-324) and others have argued that similar constraints apply to genes and proteins. They have questioned whether an undirected search via mutation and selection would have a reasonable chance of locating new islands of function--representing fundamentally new genes or proteins--within the time available (Eden 1967, Shutzenberger 1967, Lovtrup 1979). Some have also argued that alterations in sequencing would likely result in loss of protein function before fundamentally new function could arise (Eden 1967, Denton 1986). Nevertheless, neither the extent to which genes and proteins are sensitive to functional loss as a result of sequence change, nor the extent to which functional proteins are isolated within sequence space, has been fully known.

Recently, experiments in molecular biology have shed light on these questions. A variety of mutagenesis techniques have shown that proteins (and thus the genes that produce them) are indeed highly specified relative to biological function (Bowie & Sauer 1989, Reidhaar-Olson & Sauer 1990, Taylor et al. 2001). Mutagenesis research tests the sensitivity of proteins (and, by implication, DNA) to functional loss as a result of alterations in sequencing. Studies of proteins have long shown that amino acid residues at many active positions cannot vary without functional loss (Perutz & Lehmann 1968). More recent protein studies (often using mutagenesis experiments) have shown that functional requirements place significant constraints on sequencing even at non-active site positions (Bowie & Sauer 1989, Reidhaar-Olson & Sauer 1990, Chothia et al. 1998, Axe 2000, Taylor et al. 2001). In particular, Axe (2000) has shown that multiple as opposed to single position amino acid substitutions inevitably result in loss of protein function, even when these changes occur at sites that allow variation when altered in isolation. Cumulatively, these constraints imply that proteins are highly sensitive to functional loss as a result of alterations in sequencing, and that functional proteins represent highly isolated and improbable arrangements of amino acids -arrangements that are far more improbable, in fact, than would be likely to arise by chance alone in the time available (Reidhaar-Olson & Sauer 1990; Behe 1992; Kauffman 1995:44; Dembski 1998:175-223; Axe 2000, 2004). (See below the discussion of the neutral theory of evolution for a precise quantitative assessment.)

Of course, neo-Darwinists do not envision a completely random search through the set of all possible nucleotide sequences--so-called “sequence space.” They envision natural selection acting to preserve small advantageous variations in genetic sequences and their corresponding protein products. Dawkins (1996), for example, likens an organism to a high mountain peak. He compares climbing the sheer precipice up the front side of the mountain to building a new organism by chance. He acknowledges that his approach up “Mount Improbable” will not succeed. Nevertheless, he suggests that there is a gradual slope up the backside of the mountain that could be climbed in small incremental steps. In his analogy, the backside climb up “Mount Improbable” corresponds to the process of natural selection acting on random changes in the genetic text. What chance alone cannot accomplish blindly or in one leap, selection (acting on mutations) can accomplish through the cumulative effect of many slight successive steps.

Yet the extreme specificity and complexity of proteins presents a difficulty, not only for the chance origin of specified biological information (i.e., for random mutations acting alone), but also for selection and mutation acting in concert. Indeed, mutagenesis experiments cast doubt on each of the two scenarios by which neo-Darwinists envisioned new information arising from the mutation/selection mechanism (for review, see Lonnig 2001). For neo-Darwinism, new functional genes either arise from non-coding sections in the genome or from preexisting genes. Both scenarios are problematic.

In the first scenario, neo-Darwinists envision new genetic information arising from those sections of the genetic text that can presumably vary freely without consequence to the organism. According to this scenario, non-coding sections of the genome, or duplicated sections of coding regions, can experience a protracted period of “neutral evolution” (Kimura 1983) during which alterations in nucleotide sequences have no discernible effect on the function of the organism. Eventually, however, a new gene sequence will arise that can code for a novel protein. At that point, natural selection can favor the new gene and its functional protein product, thus securing the preservation and heritability of both.

This scenario has the advantage of allowing the genome to vary through many generations, as mutations “search” the space of possible base sequences. The scenario has an overriding problem, however: the size of the combinatorial space (i.e., the number of possible amino acid sequences) and the extreme rarity and isolation of the functional sequences within that space of possibilities. Since natural selection can do nothing to help generate new functional sequences, but rather can only preserve such sequences once they have arisen, chance alone--random variation--must do the work of information generation--that is, of finding the exceedingly rare functional sequences within the set of combinatorial possibilities. Yet the probability of randomly assembling (or “finding,” in the previous sense) a functional sequence is extremely small.

Cassette mutagenesis experiments performed during the early 1990s suggest that the probability of attaining (at random) the correct sequencing for a short protein 100 amino acids long is about 1 in 10⁶⁵ (Reidhaar-Olson & Sauer 1990, Behe 1992:65-69). This result agreed closely with earlier calculations that Yockey (1978) had performed based upon the known sequence variability of cytochrome c in different species and other theoretical considerations. More recent mutagenesis research has provided additional support for the conclusion that functional proteins are exceedingly rare among possible amino acid sequences (Axe 2000, 2004). Axe (2004) has performed site directed mutagenesis experiments on a 150-residue protein-folding domain within a B-lactamase enzyme. His experimental method improves upon earlier mutagenesis techniques and corrects for several sources of possible estimation error inherent in them. On the basis of these experiments, Axe has estimated the ratio of (a) proteins of typical size (150 residues) that perform a specified function via any folded structure to (b) the whole set of possible amino acids sequences of that size. Based on his experiments, Axe has estimated his ratio to be 1 to 10⁷⁷. Thus, the probability of finding a functional protein among the possible amino acid sequences corresponding to a 150-residue protein is similarly 1 in 10⁷⁷.

Other considerations imply additional improbabilities. First, new Cambrian animals would require proteins much longer than 100 residues to perform many necessary specialized functions. Ohno (1996) has noted that Cambrian animals would have required complex proteins such as lysyl oxidase in order to support their stout body structures. Lysyl oxidase molecules in extant organisms comprise over 400 amino acids. These molecules are both highly complex (non-repetitive) and functionally specified. Reasonable extrapolation from mutagenesis experiments done on shorter protein molecules suggests that the probability of producing functionally sequenced proteins of this length at random is so small as to make appeals to chance absurd, even granting the duration of the entire universe. (See Dembski 1998:175-223 for a rigorous calculation of this “Universal Probability Bound”; See also Axe 2004.) Yet, second, fossil data (Bowring et al. 1993, 1998a:1, 1998b:40; Kerr 1993; Monatersky 1993), and even molecular analyses supporting deep divergence (Wray et al. 1996), suggest that the duration of the Cambrian explosion (between 5-10 x 10⁶ and, at most, 7 x 10⁷ years) is far smaller than that of the entire universe (1.3-2 x 10¹⁰ years). Third, DNA mutation rates are far too low to generate the novel genes and proteins necessary to building the Cambrian animals, given the most probable duration of the explosion as determined by fossil studies (Conway Morris 1998b). As Ohno (1996:8475) notes, even a mutation rate of 10-⁹ per base pair per year results in only a 1% change in the sequence of a given section of DNA in 10 million years. Thus, he argues that mutational divergence of preexisting genes cannot explain the origin of the Cambrian forms in that time.⁴

The selection/mutation mechanism faces another probabilistic obstacle. The animals that arise in the Cambrian exhibit structures that would have required many new types of cells, each of which would have required many novel proteins to perform their specialized functions. Further, new cell types require Asystems of proteins that must, as a condition of functioning, act in close coordination with one another. The unit of selection in such systems ascends to the system as a whole. Natural selection selects for functional advantage. But new cell types require whole systems of proteins to perform their distinctive functions. In such cases, natural selection cannot contribute to the process of information generation until after the information necessary to build the requisite system of proteins has arisen. Thus random variations must, again, do the work of information generation--and now not simply for one protein, but for many proteins arising at nearly the same time. Yet the odds of this occurring by chance alone are, of course, far smaller than the odds of the chance origin of a single gene or protein--so small in fact as to render the chance origin of the genetic information necessary to build a new cell type (a necessary but not sufficient condition of building a new body plan) problematic given even the most optimistic estimates for the duration of the Cambrian explosion.

Dawkins (1986:139) has noted that scientific theories can rely on only so much “luck” before they cease to be credible. The neutral theory of evolution, which, by its own logic, prevents natural selection from playing a role in generating genetic information until after the fact, relies on entirely too much luck. The sensitivity of proteins to functional loss, the need for long proteins to build new cell types and animals, the need for whole new systems of proteins to service new cell types, the probable brevity of the Cambrian explosion relative to mutation rates--all suggest the immense improbability (and implausibility) of any scenario for the origination of Cambrian genetic information that relies upon random variation alone unassisted by natural selection.

Yet the neutral theory requires novel genes and proteins to arise--essentially--by random mutation alone. Adaptive advantage accrues after the generation of new functional genes and proteins. Thus, natural selection cannot play a role until new information-bearing molecules have independently arisen. Thus neutral theorists envisioned the need to scale the steep face of a Dawkins-style precipice of which there is no gradually sloping backside--a situation that, by Dawkins' own logic, is probabilistically untenable.

In the second scenario, neo-Darwinists envisioned novel genes and proteins arising by numerous successive mutations in the preexisting genetic text that codes for proteins. To adapt Dawkins's metaphor, this scenario envisions gradually climbing down one functional peak and then ascending another. Yet mutagenesis experiments again suggest a difficulty. Recent experiments show that, even when exploring a region of sequence space populated by proteins of a single fold and function, most multiple-position changes quickly lead to loss of function (Axe 2000). Yet to turn one protein into another with a completely novel structure and function requires specified changes at many sites. Indeed, the number of changes necessary to produce a new protein greatly exceeds the number of changes that will typically produce functional losses. Given this, the probability of escaping total functional loss during a random search for the changes needed to produce a new function is extremely small--and this probability diminishes exponentially with each additional requisite change (Axe 2000). Thus, Axe's results imply that, in all probability, random searches for novel proteins (through sequence space) will result in functional loss long before any novel functional protein will emerge.

Blanco et al. have come to a similar conclusion. Using directed mutagenesis, they have determined that residues in both the hydrophobic core and on the surface of the protein play essential roles in determining protein structure. By sampling intermediate sequences between two naturally occurring sequences that adopt different folds, they found that the intermediate sequences “lack a well defined three-dimensional structure.” Thus, they conclude that it is unlikely that a new protein fold via a series of folded intermediates sequences (Blanco et al. 1999:741).

Thus, although this second neo-Darwinian scenario has the advantage of starting with functional genes and proteins, it also has a lethal disadvantage: any process of random mutation or rearrangement in the genome would in all probability generate nonfunctional intermediate sequences before fundamentally new functional genes or proteins would arise. Clearly, nonfunctional intermediate sequences confer no survival advantage on their host organisms. Natural selection favors only functional advantage. It cannot select or favor nucleotide sequences or polypeptide chains that do not yet perform biological functions, and still less will it favor sequences that efface or destroy preexisting function.

Evolving genes and proteins will range through a series of nonfunctional intermediate sequences that natural selection will not favor or preserve but will, in all probability, eliminate (Blanco et al. 1999, Axe 2000). When this happens, selection-driven evolution will cease. At this point, neutral evolution of the genome (unhinged from selective pressure) may ensue, but, as we have seen, such a process must overcome immense probabilistic hurdles, even granting cosmic time.

Thus, whether one envisions the evolutionary process beginning with a noncoding region of the genome or a preexisting functional gene, the functional specificity and complexity of proteins impose very stringent limitations on the efficacy of mutation and selection. In the first case, function must arise first, before natural selection can act to favor a novel variation. In the second case, function must be continuously maintained in order to prevent deleterious (or lethal) consequences to the organism and to allow further evolution. Yet the complexity and functional specificity of proteins implies that both these conditions will be extremely difficult to meet. Therefore, the neo-Darwinian mechanism appears to be inadequate to generate the new information present in the novel genes and proteins that arise with the Cambrian animals.

Novel Body Plans

The problems with the neo-Darwinian mechanism run deeper still. In order to explain the origin of the Cambrian animals, one must account not only for new proteins and cell types, but also for the origin of new body plans. Within the past decade, developmental biology has dramatically advanced our understanding of how body plans are built during ontogeny. In the process, it has also uncovered a profound difficulty for neo-Darwinism.

Significant morphological change in organisms requires attention to timing. Mutations in genes that are expressed late in the development of an organism will not affect the body plan. Mutations expressed early in development, however, could conceivably produce significant morphological change (Arthur 1997:21). Thus, events expressed early in the development of organisms have the only realistic chance of producing large-scale macroevolutionary change (Thomson 1992). As John and Miklos (1988:309) explain, macroevolutionary change requires alterations in the very early stages of ontogenesis.

Yet recent studies in developmental biology make clear that mutations expressed early in development typically have deleterious effects (Arthur 1997:21). For example, when early-acting body plan molecules, or morphogens such as bicoid (which helps to set up the anterior-posterior head-to-tail axis in Drosophila), are perturbed, development shuts down (Nusslein-Volhard & Wieschaus 1980, Lawrence & Struhl 1996, Muller & Newman 2003).⁵ The resulting embryos die. Moreover, there is a good reason for this. If an engineer modifies the length of the piston rods in an internal combustion engine without modifying the crankshaft accordingly, the engine won't start. Similarly, processes of development are tightly integrated spatially and temporally such that changes early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream. For this reason, mutations will be much more likely to be deadly if they disrupt a functionally deeply-embedded structure such as a spinal column than if they affect more isolated anatomical features such as fingers (Kauffman 1995:200).

This problem has led to what McDonald (1983) has called “a great Darwinian paradox” (p. 93). McDonald notes that genes that are observed to vary within natural populations do not lead to major adaptive changes, while genes that could cause major changes--the very stuff of macroevolution--apparently do not vary. In other words, mutations of the kind that macroevolution doesn't need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don't occur.⁶ According to Darwin (1859:108) natural selection cannot act until favorable variations arise in a population. Yet there is no evidence from developmental genetics that the kind of variations required by neo-Darwinism--namely, favorable body plan mutations--ever occur.

Developmental biology has raised another formidable problem for the mutation/selection mechanism. Embryological evidence has long shown that DNA does not wholly determine morphological form (Goodwin 1985, Nijhout 1990, Sapp 1987, Muller & Newman 2003), suggesting that mutations in DNA alone cannot account for the morphological changes required to build a new body plan.

DNA helps direct protein synthesis.⁷ It also helps to regulate the timing and expression of the synthesis of various proteins within cells. Yet, DNA alone does not determine how individual proteins assemble themselves into larger systems of proteins; still less does it solely determine how cell types, tissue types, and organs arrange themselves into body plans (Harold 1995:2774, Moss 2004). Instead, other factors--such as the three-dimensional structure and organization of the cell membrane and cytoskeleton and the spatial architecture of the fertilized egg--play important roles in determining body plan formation during embryogenesis.

For example, the structure and location of the cytoskeleton influence the patterning of embryos. Arrays of microtubules help to distribute the essential proteins used during development to their correct locations in the cell. Of course, microtubules themselves are made of many protein subunits. Nevertheless, like bricks that can be used to assemble many different structures, the tubulin subunits in the cell's microtubules are identical to one another. Thus, neither the tubulin subunits nor the genes that produce them account for the different shape of microtubule arrays that distinguish different kinds of embryos and developmental pathways. Instead, the structure of the microtubule array itself is determined by the location and arrangement of its subunits, not the properties of the subunits themselves. For this reason, it is not possible to predict the structure of the cytoskeleton of the cell from the characteristics of the protein constituents that form that structure (Harold 2001:125).

Two analogies may help further clarify the point. At a building site, builders will make use of many materials: lumber, wires, nails, drywall, piping, and windows. Yet building materials do not determine the floor plan of the house, or the arrangement of houses in a neighborhood. Similarly, electronic circuits are composed of many components, such as resistors, capacitors, and transistors. But such lower-level components do not determine their own arrangement in an integrated circuit. Biological symptoms also depend on hierarchical arrangements of parts. Genes and proteins are made from simple building blocks--nucleotide bases and amino acids--arranged in specific ways. Cell types are made of, among other things, systems of specialized proteins. Organs are made of specialized arrangements of cell types and tissues. And body plans comprise specific arrangements of specialized organs. Yet, clearly, the properties of individual proteins (or, indeed, the lower-level parts in the hierarchy generally) do not fully determine the organization of the higher-level structures and organizational patterns (Harold 2001:125). It follows that the genetic information that codes for proteins does not determine these higher-level structures either.

These considerations pose another challenge to the sufficiency of the neo-Darwinian mechanism. Neo-Darwinism seeks to explain the origin of new information, form, and structure as a result of selection acting on randomly arising variation at a very low level within the biological hierarchy, namely, within the genetic text. Yet major morphological innovations depend on a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. Yet if DNA is not wholly responsible for body plan morphogenesis, then DNA sequences can mutate indefinitely, without regard to realistic probabilistic limits, and still not produce a new body plan. Thus, the mechanism of natural selection acting on random mutations in DNA cannot in principle generate novel body plans, including those that first arose in the Cambrian explosion.

Of course, it could be argued that, while many single proteins do not by themselves determine cellular structures and/or body plans, proteins acting in concert with other proteins or suites of proteins could determine such higher-level form. For example, it might be pointed out that the tubulin subunits (cited above) are assembled by other helper proteins--gene products--called Microtubule Associated Proteins (MAPS). This might seem to suggest that genes and gene products alone do suffice to determine the development of the three-dimensional structure of the cytoskeleton.

Yet MAPS, and indeed many other necessary proteins, are only part of the story. The location of specified target sites on the interior of the cell membrane also helps to determine the shape of the cytoskeleton. Similarly, so does the position and structure of the centrosome which nucleates the microtubules that form the cytoskeleton. While both the membrane targets and the centrosomes are made of proteins, the location and form of these structures is not wholly determined by the proteins that form them. Indeed, centrosome structure and membrane patterns as a whole convey three-dimensional structural information that helps determine the structure of the cytoskeleton and the location of its subunits (McNiven & Porter 1992:313-329). Moreover, the centrioles that compose the centrosomes replicate independently of DNA replication (Lange et al. 2000:235-249, Marshall & Rosenbaum 2000:187-205). The daughter centriole receives its form from the overall structure of the mother centriole, not from the individual gene products that constitute it (Lange et al. 2000). In ciliates, microsurgery on cell membranes can produce heritable changes in membrane patterns, even though the DNA of the ciliates has not been altered (Sonneborn 1970:1-13, Frankel 1980:607-623; Nanney 1983:163-170). This suggests that membrane patterns (as opposed to membrane constituents) are impressed directly on daughter cells. In both cases, form is transmitted from parent three-dimensional structures to daughter three-dimensional structures directly and is not wholly contained in constituent proteins or genetic information (Moss 2004).

Thus, in each new generation, the form and structure of the cell arises as the result of both gene products and preexisting three-dimensional structure and organization. Cellular structures are built from proteins, but proteins find their way to correct locations in part because of preexisting three-dimensional patterns and organization inherent in cellular structures. Preexisting three-dimensional form present in the preceding generation (whether inherent in the cell membrane, the centrosomes, the cytoskeleton or other features of the fertilized egg) contributes to the production of form in the next generation. Neither structural proteins alone, nor the genes that code for them, are sufficient to determine the three-dimensional shape and structure of the entities they form. Gene products provide necessary, but not sufficient conditions, for the development of three-dimensional structure within cells, organs and body plans (Harold 1995:2767). But if this is so, then natural selection acting on genetic variation alone cannot produce the new forms that arise in history of life.

Self-Organizational Models

Of course, neo-Darwinism is not the only evolutionary theory for explaining the origin of novel biological form. Kauffman (1995) doubts the efficacy of the mutation/selection mechanism. Nevertheless, he has advanced a self-organizational theory to account for the emergence of new form, and presumably the information necessary to generate it. Whereas neo-Darwinism attempts to explain new form as the consequence of selection acting on random mutation, Kauffman suggests that selection acts, not mainly on random variations, but on emergent patterns of order that self-organize via the laws of nature.

Kauffman (1995:47-92) illustrates how this might work with various model systems in a computer environment. In one, he conceives a system of buttons connected by strings. Buttons represent novel genes or gene products; strings represent the law-like forces of interaction that obtain between gene products-i.e., proteins. Kauffman suggests that when the complexity of the system (as represented by the number of buttons and strings) reaches a critical threshold, new modes of organization can arise in the system “for free”--that is, naturally and spontaneously--after the manner of a phase transition in chemistry.

Another model that Kauffman develops is a system of interconnected lights. Each light can flash in a variety of states--on, off, twinkling, etc. Since there is more than one possible state for each light, and many lights, there are a vast number of possible states that the system can adopt. Further, in his system, rules determine how past states will influence future states. Kauffman asserts that, as a result of these rules, the system will, if properly tuned, eventually produce a kind of order in which a few basic patterns of light activity recur with greater-than-random frequency. Since these actual patterns of light activity represent a small portion of the total number of possible states in which the system can reside, Kauffman seems to imply that self-organizational laws might similarly result in highly improbable biological outcomes--perhaps even sequences (of bases or amino acids) within a much larger sequence space of possibilities.

Do these simulations of self-organizational processes accurately model the origin of novel genetic information? It is hard to think so.

First, in both examples, Kauffman presupposes but does not explain significant sources of preexisting information. In his buttons-and-strings system, the buttons represent proteins, themselves packets of CSI, and the result of preexisting genetic information. Where does this information come from? Kauffman (1995) doesn't say, but the origin of such information is an essential part of what needs to be explained in the history of life. Similarly, in his light system, the order that allegedly arises for “for free” actually arises only if the programmer of the model system “tunes” it in such a way as to keep it from either (a) generating an excessively rigid order or (b) developing into chaos (pp. 86-88). Yet this necessary tuning involves an intelligent programmer selecting certain parameters and excluding others--that is, inputting information.

Second, Kauffman's model systems are not constrained by functional considerations and thus are not analogous to biological systems. A system of interconnected lights governed by pre-programmed rules may well settle into a small number of patterns within a much larger space of possibilities. But because these patterns have no function, and need not meet any functional requirements, they have no specificity analogous to that present in actual organisms. Instead, examination of Kauffman's (1995) model systems shows that they do not produce sequences or systems characterized by specified complexity, but instead by large amounts of symmetrical order or internal redundancy interspersed with aperiodicity or (mere) complexity (pp. 53, 89, 102). Getting a law-governed system to generate repetitive patterns of flashing lights, even with a certain amount of variation, is clearly interesting, but not biologically relevant. On the other hand, a system of lights flashing the title of a Broadway play would model a biologically relevant self-organizational process, at least if such a meaningful or functionally specified sequence arose without intelligent agents previously programming the system with equivalent amounts of CSI. In any case, Kauffman's systems do not produce specified complexity, and thus do not offer promising models for explaining the new genes and proteins that arose in the Cambrian.

Even so, Kauffman suggests that his self-organizational models can specifically elucidate aspects of the Cambrian explosion. According to Kauffman (1995:199-201), new Cambrian animals emerged as the result of “long jump” mutations that established new body plans in a discrete rather than gradual fashion. He also recognizes that mutations affecting early development are almost inevitably harmful. Thus, he concludes that body plans, once established, will not change, and that any subsequent evolution must occur within an established body plan (Kauffman 1995:201). And indeed, the fossil record does show a curious (from a neo-Darwinian point of view) top-down pattern of appearance, in which higher taxa (and the body plans they represent) appear first, only later to be followed by the multiplication of lower taxa representing variations within those original body designs (Erwin et al. 1987, Lewin 1988, Valentine & Jablonski 2003:518). Further, as Kauffman expects, body plans appear suddenly and persist without significant modification over time.

But here, again, Kauffman begs the most important question, which is: what produces the new Cambrian body plans in the first place? Granted, he invokes “long jump mutations” to explain this, but he identifies no specific self-organizational process that can produce such mutations. Moreover, he concedes a principle that undermines the plausibility of his own proposal. Kauffman acknowledges that mutations that occur early in development are almost inevitably deleterious. Yet developmental biologists know that these are the only kind of mutations that have a realistic chance of producing large-scale evolutionary change--i.e., the big jumps that Kauffman invokes. Though Kauffman repudiates the neo-Darwinian reliance upon random mutations in favor of self-organizing order, in the end, he must invoke the most implausible kind of random mutation in order to provide a self-organizational account of the new Cambrian body plans. Clearly, his model is not sufficient.

Punctuated Equilibrium

Of course, still other causal explanations have been proposed. During the 1970s, the paleontologists Eldredge and Gould (1972) proposed the theory of evolution by punctuated equilibrium in order to account for a pervasive pattern of “sudden appearance” and “stasis” in the fossil record. Though advocates of punctuated equilibrium were mainly seeking to describe the fossil record more accurately than earlier gradualist neo-Darwinian models had done, they did also propose a mechanism--known as species selection--by which the large morphological jumps evident in fossil record might have been produced. According to punctuationalists, natural selection functions more as a mechanism for selecting the fittest species rather than the most-fit individual among a species. Accordingly, on this model, morphological change should occur in larger, more discrete intervals than it would given a traditional neo-Darwinian understanding.

Despite its virtues as a descriptive model of the history of life, punctuated equilibrium has been widely criticized for failing to provide a mechanism sufficient to produce the novel form characteristic of higher taxonomic groups. For one thing, critics have noted that the proposed mechanism of punctuated evolutionary change simply lacked the raw material upon which to work. As Valentine and Erwin (1987) note, the fossil record fails to document a large pool of species prior to the Cambrian. Yet the proposed mechanism of species selection requires just such a pool of species upon which to act. Thus, they conclude that the mechanism of species selection probably does not resolve the problem of the origin of the higher taxonomic groups (p. 96).⁸ Further, punctuated equilibrium has not addressed the more specific and fundamental problem of explaining the origin of the new biological information (whether genetic or epigenetic) necessary to produce novel biological form. Advocates of punctuated equilibrium might assume that the new species (upon which natural selection acts) arise by known microevolutionary processes of speciation (such as founder effect, genetic drift or bottleneck effect) that do not necessarily depend upon mutations to produce adaptive changes. But, in that case, the theory lacks an account of how the specifically higher taxa arise. Species selection will only produce more fit species. On the other hand, if punctuationalists assume that processes of genetic mutation can produce more fundamental morphological changes and variations, then their model becomes subject to the same problems as neo-Darwinism (see above). This dilemma is evident in Gould (2002:710) insofar as his attempts to explain adaptive complexity inevitably employ classical neo-Darwinian modes of explanation^.9

Structuralism

Another attempt to explain the origin of form has been proposed by the structuralists such as Gerry Webster and Brian Goodwin (1984, 1996). These biologists, drawing on the earlier work of D'Arcy Thompson (1942), view biological form as the result of structural constraints imposed upon matter by morphogenetic rules or laws. For reasons similar to those discussed above, the structuralists have insisted that these generative or morphogenetic rules do not reside in the lower level building materials of organisms, whether in genes or proteins. Webster and Goodwin (1984:510-511) further envisioned morphogenetic rules or laws operating ahistorically, similar to the way in which gravitational or electromagnetic laws operate. For this reason, structuralists see phylogeny as of secondary importance in understanding the origin of the higher taxa, though they think that transformations of form can occur. For structuralists, constraints on the arrangement of matter arise not mainly as the result of historical contingencies--such as environmental changes or genetic mutations--but instead because of the continuous ahistorical operation of fundamental laws of form--laws that organize or inform matter.

While this approach avoids many of the difficulties currently afflicting neo-Darwinism (in particular those associated with its “genocentricity”), critics (such as Maynard Smith 1986) of structuralism have argued that the structuralist explanation of form lacks specificity. They note that structuralists have been unable to say just where laws of form reside--whether in the universe, or in every possible world, or in organisms as a whole, or in just some part of organisms. Further, according to structuralists, morphogenetic laws are mathematical in character. Yet, structuralists have yet to specify the mathematical formulae that determine biological forms.

Others (Yockey 1992; Polanyi 1967, 1968; Meyer 2003) have questioned whether physical laws could in principle generate the kind of complexity that characterizes biological systems. Structuralists envision the existence of biological laws that produce form in much the same way that physical laws produce form. Yet the forms that physicists regard as manifestations of underlying laws are characterized by large amounts of symmetric or redundant order, by relatively simple patterns such as vortices or gravitational fields or magnetic lines of force. Indeed, physical laws are typically expressed as differential equations (or algorithms) that almost by definition describe recurring phenomena--patterns of compressible “order” not “complexity” as defined by algorithmic information theory (Yockey 1992:77-83). Biological forms, by contrast, manifest greater complexity and derive in ontogeny from highly complex initial conditions--i.e., non-redundant sequences of nucleotide bases in the genome and other forms of information expressed in the complex and irregular three-dimensional topography of the organism or the fertilized egg. Thus, the kind of form that physical laws produce is not analogous to biological form--at least not when compared from the standpoint of (algorithmic) complexity. Further, physical laws lack the information content to specify biology systems. As Polyanyi (1967, 1968) and Yockey (1992:290) have shown, the laws of physics and chemistry allow, but do not determine, distinctively biological modes of organization. In other words, living systems are consistent with, but not deducible, from physical-chemical laws (1992:290).

Of course, biological systems do manifest some reoccurring patterns, processes and behaviors. The same type of organism develops repeatedly from similar ontogenetic processes in the same species. Similar processes of cell division reoccur in many organisms. Thus, one might describe certain biological processes as law-governed. Even so, the existence of such biological regularities does not solve the problem of the origin of form and information, since the recurring processes described by such biological laws (if there be such laws) only occur as the result of preexisting stores of (genetic and/or epigenetic) information and these information-rich initial conditions impose the constraints that produce the recurring behavior in biological systems. (For example, processes of cell division recur with great frequency in organisms, but depend upon information-rich DNA and proteins molecules.) In other words, distinctively biological regularities depend upon preexisting biological information. Thus, appeals to higher-level biological laws presuppose, but do not explain, the origination of the information necessary to morphogenesis.

Thus, structuralism faces a difficult in principle dilemma. On the one hand, physical laws produce very simple redundant patterns that lack the complexity characteristic of biological systems. On the other hand, distinctively biological laws--if there are such laws--depend upon preexisting information-rich structures. In either case, laws are not good candidates for explaining the origination of biological form or the information necessary to produce it.

Cladism: An Artifact of Classification?

Some cladists have advanced another approach to the problem of the origin of form, specifically as it arises in the Cambrian. They have argued that the problem of the origin of the phyla is an artifact of the classification system, and therefore, does not require explanation. Budd and Jensen (2000), for example, argue that the problem of the Cambrian explosion resolves itself if one keeps in mind the cladistic distinction between “stem” and “crown” groups. Since crown groups arise whenever new characters are added to simpler more ancestral stem groups during the evolutionary process, new phyla will inevitably arise once a new stem group has arisen. Thus, for Budd and Jensen what requires explanation is not the crown groups corresponding to the new Cambrian phyla, but the earlier more primitive stem groups that presumably arose deep in the Proterozoic. Yet since these earlier stem groups are by definition less derived, explaining them will be considerably easier than explaining the origin of the Cambrian animals de novo. In any case, for Budd and Jensen the explosion of new phyla in the Cambrian does not require explanation. As they put it, “given that the early branching points of major clades is an inevitable result of clade diversification, the alleged phenomenon of the phyla appearing early and remaining morphologically static is not seen to require particular explanation” (Budd & Jensen 2000:253).

While superficially plausible, perhaps, Budd and Jensen's attempt to explain away the Cambrian explosion begs crucial questions. Granted, as new characters are added to existing forms, novels morphology and greater morphological disparity will likely result. But what causes new characters to arise? And how does the information necessary to produce new characters originate? Budd and Jensen do not specify. Nor can they say how derived the ancestral forms are likely to have been, and what processes, might have been sufficient to produce them. Instead, they simply assume the sufficiency of known neo-Darwinian mechanisms (Budd & Jensen 2000:288). Yet, as shown above, this assumption is now problematic. In any case, Budd and Jensen do not explain what causes the origination of biological form and information.

Convergence and Teleological Evolution

More recently, Conway Morris (2000, 2003c) has suggested another possible explanation based on the tendency for evolution to converge on the same structural forms during the history of life. Conway Morris cites numerous examples of organisms that possess very similar forms and structures, even though such structures are often built from different material substrates and arise (in ontogeny) by the expression of very different genes. Given the extreme improbability of the same structures arising by random mutation and selection in disparate phylogenies, Conway Morris argues that the pervasiveness of convergent structures suggests that evolution may be in some way “channeled” toward similar functional and/or structural endpoints. Such an end-directed understanding of evolution, he admits, raises the controversial prospect of a teleological or purposive element in the history of life. For this reason, he argues that the phenomenon of convergence has received less attention than it might have otherwise. Nevertheless, he argues that just as physicists have reopened the question of design in their discussions of anthropic fine-tuning, the ubiquity of convergent structures in the history of life has led some biologists (Denton 1998) to consider extending teleological thinking to biology. And, indeed, Conway Morris himself intimates that the evolutionary process might be “underpinned by a purpose” (2000:8, 2003b:511).

Conway Morris, of course, considers this possibility in relation to a very specific aspect of the problem of organismal form, namely, the problem of explaining why the same forms arise repeatedly in so many disparate lines of decent. But this raises a question. Could a similar approach shed explanatory light on the more general causal question that has been addressed in this review? Could the notion of purposive design help provide a more adequate explanation for the origin of organismal form generally? Are there reasons to consider design as an explanation for the origin of the biological information necessary to produce the higher taxa and their corresponding morphological novelty?

The remainder of this review will suggest that there are such reasons. In so doing, it may also help explain why the issue of teleology or design has reemerged within the scientific discussion of biological origins (Denton 1986, 1998; Thaxton et al. 1992; Kenyon & Mills 1996: Behe 1996, 2004; Dembski 1998, 2002, 2004; Conway Morris 2000, 2003a, 2003b, Lonnig 2001; Lonnig & Saedler 2002; Nelson & Wells 2003; Meyer 2003, 2004; Bradley 2004) and why some scientists and philosophers of science have considered teleological explanations for the origin of form and information despite strong methodological prohibitions against design as a scientific hypothesis (Gillespie 1979, Lenior 1982:4).

First, the possibility of design as an explanation follows logically from a consideration of the deficiencies of neo-Darwinism and other current theories as explanations for some of the more striking “appearances of design” in biological systems. Neo-Darwinists such as Ayala (1994:5), Dawkins (1986:1), Mayr (1982:xi-xii) and Lewontin (1978) have long acknowledged that organisms appear to have been designed. Of course, neo-Darwinists assert that what Ayala (1994:5) calls the “obvious design” of living things is only apparent since the selection/mutation mechanism can explain the origin of complex form and organization in living systems without an appeal to a designing agent. Indeed, neo-Darwinists affirm that mutation and selection--and perhaps other similarly undirected mechanisms--are fully sufficient to explain the appearance of design in biology. Self-organizational theorists and punctuationalists modify this claim, but affirm its essential tenet. Self-organization theorists argue that natural selection acting on self organizing order can explain the complexity of living things--again, without any appeal to design. Punctuationalists similarly envision natural selection acting on newly arising species with no actual design involved.

And clearly, the neo-Darwinian mechanism does explain many appearances of design, such as the adaptation of organisms to specialized environments that attracted the interest of 19th century biologists. More specifically, known microevolutionary processes appear quite sufficient to account for changes in the size of Galapagos finch beaks that have occurred in response to variations in annual rainfall and available food supplies (Weiner 1994, Grant 1999).

But does neo-Darwinism, or any other fully materialistic model, explain all appearances of design in biology, including the body plans and information that characterize living systems? Arguably, biological forms--such as the structure of a chambered nautilus, the organization of a trilobite, the functional integration of parts in an eye or molecular machine--attract our attention in part because the organized complexity of such systems seems reminiscent of our own designs. Yet, this review has argued that neo-Darwinism does not adequately account for the origin of all appearances of design, especially if one considers animal body plans, and the information necessary to construct them, as especially striking examples of the appearance of design in living systems. Indeed, Dawkins (1995:11) and Gates (1996:228) have noted that genetic information bears an uncanny resemblance to computer software or machine code. For this reason, the presence of CSI in living organisms, and the discontinuous increases of CSI that occurred during events such as the Cambrian explosion, appears at least suggestive of design.

Does neo-Darwinism or any other purely materialistic model of morphogenesis account for the origin of the genetic and other forms of CSI necessary to produce novel organismal form? If not, as this review has argued, could the emergence of novel information-rich genes, proteins, cell types and body plans have resulted from actual design, rather than a purposeless process that merely mimics the powers of a designing intelligence? The logic of neo-Darwinism, with its specific claim to have accounted for the appearance of design, would itself seem to open the door to this possibility. Indeed, the historical formulation of Darwinism in dialectical opposition to the design hypothesis (Gillespie 1979), coupled with the neo-Darwinism's inability to account for many salient appearances of design including the emergence of form and information, would seem logically to reopen the possibility of actual (as opposed to apparent) design in the history of life.

A second reason for considering design as an explanation for these phenomena follows from the importance of explanatory power to scientific theory evaluation and from a consideration of the potential explanatory power of the design hypothesis. Studies in the methodology and philosophy of science have shown that many scientific theories, particularly in the historical sciences, are formulated and justified as inferences to the best explanation (Lipton 1991:32-88, Brush 1989:1124-1129, Sober 2000:44). Historical scientists, in particular, assess or test competing hypotheses by evaluating which hypothesis would, if true, provide the best explanation for some set of relevant data (Meyer 1991, 2002; Cleland 2001:987-989, 2002:474-496).¹⁰ Those with greater explanatory power are typically judged to be better, more probably true, theories. Darwin (1896:437) used this method of reasoning in defending his theory of universal common descent. Moreover, contemporary studies on the method of “inference to the best explanation” have shown that determining which among a set of competing possible explanations constitutes the best depends upon judgments about the causal adequacy, or “causal powers,” of competing explanatory entities (Lipton 1991:32-88). In the historical sciences, uniformitarian and/or actualistic (Gould 1965, Simpson 1970, Rutten 1971, Hooykaas 1975) canons of method suggest that judgments about causal adequacy should derive from our present knowledge of cause and effect relationships. For historical scientists, “the present is the key to the past” means that present experience-based knowledge of cause and effect relationships typically guides the assessment of the plausibility of proposed causes of past events.

Yet it is precisely for this reason that current advocates of the design hypothesis want to reconsider design as an explanation for the origin of biological form and information. This review, and much of the literature it has surveyed, suggests that four of the most prominent models for explaining the origin of biological form fail to provide adequate causal explanations for the discontinuous increases of CSI that are required to produce novel morphologies. Yet, we have repeated experience of rational and conscious agents--in particular ourselves--generating or causing increases in complex specified information, both in the form of sequence-specific lines of code and in the form of hierarchically arranged systems of parts.

In the first place, intelligent human agents--in virtue of their rationality and consciousness--have demonstrated the power to produce information in the form of linear sequence-specific arrangements of characters. Indeed, experience affirms that information of this type routinely arises from the activity of intelligent agents. A computer user who traces the information on a screen back to its source invariably comes to a mind--that of a software engineer or programmer. The information in a book or inscriptions ultimately derives from a writer or scribe--from a mental, rather than a strictly material, cause. Our experience-based knowledge of information-flow confirms that systems with large amounts of specified complexity (especially codes and languages) invariably originate from an intelligent source from a mind or personal agent. As Quastler (1964) put it, the “creation of new information is habitually associated with conscious activity” (p. 16). Experience teaches this obvious truth.

Further, the highly specified hierarchical arrangements of parts in animal body plans also suggest design, again because of our experience of the kinds of features and systems that designers can and do produce. At every level of the biological hierarchy, organisms require specified and highly improbable arrangements of lower-level constituents in order to maintain their form and function. Genes require specified arrangements of nucleotide bases; proteins require specified arrangements of amino acids; new cell types require specified arrangements of systems of proteins; body plans require specialized arrangements of cell types and organs. Organisms not only contain information-rich components (such as proteins and genes), but they comprise information-rich arrangements of those components and the systems that comprise them. Yet we know, based on our present experience of cause and effect relationships, that design engineers--possessing purposive intelligence and rationality--have the ability to produce information-rich hierarchies in which both individual modules and the arrangements of those modules exhibit complexity and specificity--information so defined. Individual transistors, resistors, and capacitors exhibit considerable complexity and specificity of design; at a higher level of organization, their specific arrangement within an integrated circuit represents additional information and reflects further design. Conscious and rational agents have, as part of their powers of purposive intelligence, the capacity to design information-rich parts and to organize those parts into functional information-rich systems and hierarchies. Further, we know of no other causal entity or process that has this capacity. Clearly, we have good reason to doubt that mutation and selection, self-organizational processes or laws of nature, can produce the information-rich components, systems, and body plans necessary to explain the origination of morphological novelty such as that which arises in the Cambrian period.

There is a third reason to consider purpose or design as an explanation for the origin of biological form and information: purposive agents have just those necessary powers that natural selection lacks as a condition of its causal adequacy. At several points in the previous analysis, we saw that natural selection lacked the ability to generate novel information precisely because it can only act after new functional CSI has arisen. Natural selection can favor new proteins, and genes, but only after they perform some function. The job of generating new functional genes, proteins and systems of proteins therefore falls entirely to random mutations. Yet without functional criteria to guide a search through the space of possible sequences, random variation is probabilistically doomed. What is needed is not just a source of variation (i.e., the freedom to search a space of possibilities) or a mode of selection that can operate after the fact of a successful search, but instead a means of selection that (a) operates during a search--before success--and that (b) is guided by information about, or knowledge of, a functional target.

Demonstration of this requirement has come from an unlikely quarter: genetic algorithms. Genetic algorithms are programs that allegedly simulate the creative power of mutation and selection. Dawkins and Kuppers, for example, have developed computer programs that putatively simulate the production of genetic information by mutation and natural selection (Dawkins 1986:47-49, Kuppers 1987:355-369). Nevertheless, as shown elsewhere (Meyer 1998:127-128, 2003:247-248), these programs only succeed by the illicit expedient of providing the computer with a “target sequence” and then treating relatively greater proximity to future function (i.e., the target sequence), not actual present function, as a selection criterion. As Berlinski (2000) has argued, genetic algorithms need something akin to a “forward looking memory” in order to succeed. Yet such foresighted selection has no analogue in nature. In biology, where differential survival depends upon maintaining function, selection cannot occur before new functional sequences arise. Natural selection lacks foresight.

What natural selection lacks, intelligent selection--purposive or goal-directed design--provides. Rational agents can arrange both matter and symbols with distant goals in mind. In using language, the human mind routinely “finds” or generates highly improbable linguistic sequences to convey an intended or preconceived idea. In the process of thought, functional objectives precede and constrain the selection of words, sounds and symbols to generate functional (and indeed meaningful) sequences from among a vast ensemble of meaningless alternative combinations of sound or symbol (Denton 1986:309-311). Similarly, the construction of complex technological objects and products, such as bridges, circuit boards, engines and software, result from the application of goal-directed constraints (Polanyi 1967, 1968). Indeed, in all functionally integrated complex systems where the cause is known by experience or observation, design engineers or other intelligent agents applied boundary constraints to limit possibilities in order to produce improbable forms, sequences or structures. Rational agents have repeatedly demonstrated the capacity to constrain the possible to actualize improbable but initially unrealized future functions. Repeated experience affirms that intelligent agents (minds) uniquely possess such causal powers.

Analysis of the problem of the origin of biological information, therefore, exposes a deficiency in the causal powers of natural selection that corresponds precisely to powers that agents are uniquely known to possess. Intelligent agents have foresight. Such agents can select functional goals before they exist. They can devise or select material means to accomplish those ends from among an array of possibilities and then actualize those goals in accord with a preconceived design plan or set of functional requirements. Rational agents can constrain combinatorial space with distant outcomes in mind. The causal powers that natural selection lacks--almost by definition--are associated with the attributes of consciousness and rationality--with purposive intelligence. Thus, by invoking design to explain the origin of new biological information, contemporary design theorists are not positing an arbitrary explanatory element unmotivated by a consideration of the evidence. Instead, they are positing an entity possessing precisely the attributes and causal powers that the phenomenon in question requires as a condition of its production and explanation.

Conclusion

An experience-based analysis of the causal powers of various explanatory hypotheses suggests purposive or intelligent design as a causally adequate--and perhaps the most causally adequate--explanation for the origin of the complex specified information required to build the Cambrian animals and the novel forms they represent. For this reason, recent scientific interest in the design hypothesis is unlikely to abate as biologists continue to wrestle with the problem of the origination of biological form and the higher taxa.


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End Notes

¹ Specifically, Gilbert et al. (1996) argued that changes in morphogenetic fields might produce large-scale changes in the developmental programs and, ultimately, body plans of organisms. Yet they offered no evidence that such fields--if indeed they exist--can be altered to produce advantageous variations in body plan, though this is a necessary condition of any successful causal theory of macroevolution.

² If one takes the fossil record at face value and assumes that the Cambrian explosion took place within a relatively narrow 5-10 million year window, explaining the origin of the information necessary to produce new proteins, for example, becomes more acute in part because mutation rates would not have been sufficient to generate the number of changes in the genome necessary to build the new proteins for more complex Cambrian animals (Ohno 1996:8475-8478). This review will argue that, even if one allows several hundred million years for the origin of the metazoan, significant probabilistic and other difficulties remain with the neo-Darwinian explanation of the origin of form and information.

³ As Crick put it, “information means here the precise determination of sequence, either of bases in the nucleic acid or on amino acid residues in the protein” (Crick 1958:144, 153).

⁴ To solve this problem Ohno himself proposes the existence of a hypothetical ancestral form that possessed virtually all the genetic information necessary to produce the new body plans of the Cambrian animals. He asserts that this ancestor and its “pananimalian genome” might have arisen several hundred million years before the Cambrian explosion. On this view, each of the different Cambrian animals would have possessed virtually identical genomes, albeit with considerable latent and unexpressed capacity in the case of each individual form (Ohno 1996:8475-8478). While this proposal might help explain the origin of the Cambrian animal forms by reference to preexisting genetic information, it does not solve, but instead merely displaces, the problem of the origin of the genetic information necessary to produce these new forms.

⁵ Some have suggested that mutations in “master regulator” Hox genes might provide the raw material for body plan morphogenesis. Yet there are two problems with this proposal. First, Hox gene expression begins only after the foundation of the body plan has been established in early embryogenesis. (Davidson 2001:66). Second, Hox genes are highly conserved across many disparate phyla and so cannot account for the morphological differences that exist between the phyla (Valentine 2004:88).

⁶ Notable differences in the developmental pathways of similar organisms have been observed. For example, congeneric species of sea urchins (from genus Heliocidaris) exhibit striking differences in their developmental pathways (Raff 1999:110-121). Thus, it might be argued that such differences show that early developmental programs can in fact be mutated to produce new forms. Nevertheless, there are two problems with this claim. First, there is no direct evidence that existing differences in sea urchin development arose by mutation. Second, the observed differences in the developmental programs of different species of sea urchins do not result in new body plans, but instead in highly conserved structures. Despite differences in developmental patterns, the endpoints are the same. Thus, even if it can be assumed that mutations produced the differences in developmental pathways, it must be acknowledged that such changes did not result in novel form.

⁷ Of course, many post-translation processes of modification also play a role in producing a functional protein. Such processes make it impossible to predict a protein's final sequencing from its corresponding gene sequence alone (Sarkar 1996:199-202).

⁸ Erwin (2004:21), although friendly to the possibility of species selection, argues that Gould provides little evidence for its existence. “The difficulty” writes Erwin of species selection, “...is that we must rely on Gould's arguments for theoretical plausibility and sufficient relative frequency. Rarely is a mass of data presented to justify and support Gould's conclusion.” Indeed, Gould (2002) himself admitted that species selection remains largely a hypothetical construct: “I freely admit that well-documented cases of species selection do not permeate the literature” (p. 710).

⁹”I do not deny either the wonder, or the powerful importance, of organized adaptive complexity. I recognize that we know no mechanism for the origin of such organismal features other than conventional natural selection at the organismic level--for the sheer intricacy and elaboration of good biomechanical design surely precludes either random production, or incidental origin as a side consequence of active processes at other levels” (Gould 2002:710). “Thus, we do not challenge the efficacy or the cardinal importance of organismal selection. As previously discussed, I fully agree with Dawkins (1986) and others that one cannot invoke a higher-level force like species selection to explain 'things that organisms do'--in particular, the stunning panoply of organismic adaptations that has always motivated our sense of wonder about the natural world, and that Darwin (1859) described, in one of his most famous lines (3), as 'that perfection of structure and coadaptation which most justly excites our admiration'“ (Gould 2002:886).

¹⁰ Theories in the historical sciences typically make claims about what happened in the past, or what happened in the past to cause particular events to occur (Meyer 1991:57-72). For this reason, historical scientific theories are rarely tested by making predictions about what will occur under controlled laboratory conditions (Cleland 2001:987, 2002:474-496). Instead, such theories are usually tested by comparing their explanatory power against that of their competitors with respect to already known facts. Even in the case in which historical theories make claims about past causes they usually do so on the basis of preexisting knowledge of cause and effect relationships. Nevertheless, prediction may play a limited role in testing historical scientific theories since such theories may have implications as to what kind of evidence is likely to emerge in the future. For example, neo-Darwinism affirms that new functional sections of the genome arise by trial and error process of mutation and subsequent selection. For this reason, historically many neo-Darwinists expected or predicted that the large non-coding regions of the genome--so-called “junk DNA”--would lack function altogether (Orgel & Crick 1980). On this line of thinking, the nonfunctional sections of the genome represent nature's failed experiments that remain in the genome as a kind of artifact of the past activity of the mutation and selection process. Advocates of the design hypotheses on the other hand, would have predicted that non-coding regions of the genome might well reveal hidden functions, not only because design theorists do not think that new genetic information arises by a trial and error process of mutation and selection, but also because designed systems are often functionally polyvalent. Even so, as new studies reveal more about the functions performed by the non-coding regions of the genome (Gibbs 2003), the design hypothesis can no longer be said to make this claim in the form of a specifically future-oriented prediction. Instead, the design hypothesis might be said to gain confirmation or support from its ability to explain this now known evidence, albeit after the fact. Of course, neo Darwinists might also amend their original prediction using various auxiliary hypotheses to explain away the presence of newly discovered functions in the non-coding regions of DNA. In both cases, considerations of ex post facto explanatory power reemerge as central to assessing and testing competing historical theories.

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[Ichneumon]

Is this the new Evo strategy if you don't like the article start something like you did in post 36 & 33 and then try to get the thread banned by running to the moderators?

Look, son, if anything happens to your thread because *you* made false accusations that you refused to either retract or try to support, even when specifically requested to do so, don't come crying to *us*, and don't blame it on the "Evos". You've dug your own hole.

And I didn't "start" anything in posts #33 and #36. *You* started something by posting blatant, transparent falsehoods. In posts #33 and #36 I called you on them and pointed out that they were, indeed, falsehoods. If the truth hurts, I'm not terribly sorry.

[Ichneumon]

No, he has actually been using this one for quite a while.

Oh look, another false accusation by a creationist. Why am I not surprised?

Let's add you to the list: Support this slur, or retract it. Where exactly do you fantasize that I have "used this strategy for quite a while" in order to get threads banned? Or at all, for that matter?

Sorry, kid, but I don't try to get threads banned at all. I'd rather shine the light of information on them and show the lurkers just how devoid of knowledge and integrity you folks are, so that people will know to "consider the source" and be less likely to swallow the propaganda next time they hear it.

Like for instance, let's consider just a *small* sampling of the ways in which creationists have spread misrepresentations (from a previous post of mine):

Summary of the ability of the two creationists (Hovind and Havoc) to present information they *know* is false, and to *fail* to retract when reminded of their falsehoods, is presented here, along with links to all appropriate documentation.

This sort of behavior, unfortunately, is *typical* of creationists. Here, want dozens of more examples of their distortions? A few more for the road? Another? Still more, perhaps? How about even more? Ooh, here are some good examples. And there's lots more where that came from, like this and this and this and lots more here and *tons* here and countless more here and yet more here, a goodie... Wait, there's more over here, etc., etc., etc., etc., etc., *ETC.*, etc., etc., etc., . How about 300 more creationist misrepresentations? Not enough, you say? Well then visit Creationist Lies and Blunders. Hey, what about Freeper metacognative's (he's a creationist) ability to accuse Daniel Dennett (evolutionary scientist) of wanting to put Christians into concentration camps for their beliefs, when Dennett was *actually* clearly writing about how RADICAL ISLAM may need to be contained? The ugly details here. Metacognative *still* shows no shame for his patently false accusation.

Tell me, microgood: Do you condone this behavior of creationists? Yes or no? Is lying for the "cause" of creationism acceptable to you?

[Ichneumon]

DannyTN: [Creationists have been seeing complete sh!t published in peer reviewed so-called scientific journals for decades.]

Ichneumon: [Oh really? Cite five examples. If you can't, then you've just exposed yourself as willing to shoot off at the mouth without substantiation.]

DannyTN: Just five?

Five would do.

1. Piltdown man

Not published in a peer-reviewed journal. Strike one

2. Haeckels embryos

Not published in a peer-reviewed journal. Strike two

3. Archaeoraptor

Not published in a peer-reviewed journal. Strike three

4. Brontosaurus

Not published in a peer-reviewed journal. Strike four

5. Lucy's flat face and upright posture

What about them? Sure, creationists make various false accusations against the "Lucy" specimens, but that hardly counts as support of "sh!t" in peer-reviewed journals. Strike five

6. Nebraska man

Not published in a peer-reviewed journal. Strike six

7. Java Man

The "Java Man" specimens are legimate Homo erectus specimens, false creationist accusations notwithstanding. No "sh!t". Strike seven

8. Orce man

There's a lively debate on whether the small fragment of bone found at Orce is from a human or not. The peer-reviewed journals carry this debate. The most recent papers appear to support the human side of the debate, such as the . You claimed to have examples of "complete sh!t", but this isn't it. It's just an open question. Strike eight

9. European Neanderthal dates

There's no doubt that Protsch was a fraud who just made up dates for specimens instead of properly testing them (and sold for cash a lot of specimens that didn't belong to him, and arranged to have a lot of Nazi historical documents shredded -- he was a real piece of work), but that doesn't make all dating of European Neanderthals "complete sh!t", as you so charmingly put it. Nonetheless, I'll give you this one if you can actually identify an article in a peer-reviewed journal which unwittingly used any date which Protsch screwed up.

10. Horse evolution series

There's nothing wrong with the horse evolution series, creationist lies to the contrary notwithstanding. Strike nine

Wow, nine strikes out of ten (and one ball still up the air until you provide actual citations) -- that batting average *sucks*. Are you sure you know what in the heck you're talking about?

Sorry I couldn't stop at five.

you couldn't even get off the ground. If you were playing baseball, you'd have gotten three "outs" for your team all by yourself and you'd be off the field.

Every day we see claims attributed to evolution by scientists,

Indeed we do, backed up by mountains of evidence and endless experiments.

who are clearly just speculating and have no proof to back up their claims whatsoever.

Sorry, son, but *you're* the one who utterly failed to support your claim when challenged. Scientists can actually support their claims, even though you can't. And your over-the-top lying about them (falsely accusing them of having "no proof to back up their claims 'whatsoever'") really does nothing to help your credibility at all. You really aren't allowed to just make up things and post them -- that's called lying.

[Ichneumon]

You constantly call Creationists liars

Because it's true, as I constantly document.

and you're the biggest one.

You have yet to identify a single lie I've allegedly told, much less made a case that I'm the "biggest" liar (and in order to be the "biggest" liar in comparison to the creationists, that's *really* saying something...)

So here's your last chance to do the honorable thing, if you're at all capable of it: Actually support your slander against me, or retract it. If not, we'll see what the moderators have to say about your behavior.

[Thatcherite]

What is a good question but I find why to be ever so much more interesting. Why, for instance, does life try so dang hard to survive?

Things which "try hard" to survive are more likely to be prominent in the biosphere than things that don't.

[Selkie]

1) Intelligent Design is not creationism. "
Agreed. However, one must ask why an intelligent designer would design us and then leave us with no contact.>

Because we are supposed to grow and focus on each other in this realm, God doesn't want blind automatons obsessed with Him.
While we're alive if contact with God was a constant given, we wouldn't strive and push ourselves nearly so much.
Nor would we cling and crave the contact of fellow humans so dearly.
I think it's much more interesting this way.


PAX

[DannyTN]

1. Piltdown man : Not published in a peer-reviewed journal. Strike one

And you have the gall to call me a liar????

REPORTS ON THE FINDS: 1912-1917

 

Geological Society Papers

The "discoveries" of what had actually been fabricated and planted were reported to

the Geological Society of London in four papers, delivered by two or all three

of the major investigators: Charles Dawson, Arthur Smith Woodward, and Elliot

Smith.

 

• On the Discovery of a Palæolithic Human Skull and Mandible.(1913)

Dawson, Woodward, and Elliot Smith, talk delivered Dec. 1912 at Geological Society on first finds

• Supplementary Note on the Discovery (1914)

Dawson, Woodward and Elliot Smith on finds of 1913:

• On a Bone Implement from Piltdown (Sussex)(1914)

Dawson and Woodward on the last find from the pit, an implement made from an elephant femur to look like a cricket bat

• Fourth Note on the Piltdown Gravel (1917)

Woodward and Elliot Smith on "evidence of a second skull" at Sheffield Park

 

Relevant publications by

 

Charles Dawson

The Piltdown Skull. (Eoanthropus dawsoni ). (1913)

The "Restoratios" of the Bayeux Tapestry. (1907)

Prehistoric Remains. History of Hastings Castle (1909)

 

Arthur Smith Woodward.

Note on the Piltdown Man. (1913)

Woodward, Sherborne Horse's Head. et al. Letters to Nature   (1926)

The Second Piltdown Skull. (1933)

The Earliest Englishman. (1948)

B.B. G[ardiner] . Lady Smith Woodward's tablecloth. (1987)

+ letter from George Gaylord Simpson history of this tablecloth and of the hoax, with suggestions on suspects

On an Apparently Palæolithic Engraving.(1914)

Woodward on find of a horse's head, which was probably another hoax he fell for

C. B. Stringer, et al. Solution for the Sherborne Problem (1995)

not by Woodward, but relevant to this event - fake a recent one

On the Lower Jaw of an Anthropoid Ape [Dryopithecus].

Woodward providing background with description of a fossil primate (1914)

Keith, Smith, Woodward, Duckworth on The Fossil Anthropoid Ape from Taungs. (1925)

The Second Piltdown Skull. letter to Nature (1933)

The Earliest Englishman in its entirety (1948)

 

 

Lewis Abbott

This CD-ROM presents the only (though partial) anthology of Lewis Abbott publications.

The Section Exposed in the Foundations of the New Admiralty Offices. (1892)

Plateau Man in Kent. (1894 )

The New Oban Cave.(1895)

"diminutive Forms of Flint Implements from Hastings Kitchen Midden and Sevenoaks."

Worked Flints from the Cromer Forest Bed. (1897).

Primeval Refuse Heaps at Hastings. 2 parts, (1897)

ƒ On the Classification of the British Stone Age Industries (1911)

Pre-Historic Man: The Newly-Discovered Link in His Evolution. (1913)

The Piltdown Skull. Letter to the Editor of the Morning Post (1914)

The Discovery of British Palaeoglyphs 1914.

Abbott Letters

includes letter ( n.d.) from Ian Langham and 1981 and 1984 letters from Glyn Daniel

to C. Blinderman

 

Barlow ?

 

W. Ruskin Butterfield

Folk-names for Marine Fishes and Other Animals at Hastings. Hastings and St. Leonards Observer ( August 1913)

 

Teilhard de Chardin

ƒ The Case of Piltdown Man. (1920)

• Status of Australopithecines. On the Zoological Position and the Evolutionary

Significance of Australopithecines (1953)

other hominds, but no mention of Piltdown

The Idea of Fossil ManKroeber, A. L. (1953). Only one very quick mention of Piltdown

K. Oakley and T. de Chardin. L'Oeuvre Scientique (1971)

correspondence between Kenneth Oakley and Pierre Teilhard de Chardin on Teilhard’s remembering Piltdown case, includes letter from K. Oakley to C. Blinderman

 

Arthur Conan Doyle

Challenger and Other Fossils. The Lost World (1912)

 

J. T. Hewitt

Note on the Natural Gas at Healthfield Station (1898)

 

Martin A. C. Hinton

The Pleistocene Mammalia of the British Isles and Their Bearing upon the Date of the Glacial Period Proceedings of the Yorkshire Geological Society (1926)

Piltdown mentioned in paper read before British Association on Pleistocene mammals

Arthur Keith

• 1913 debate in Nature between Elliot Smith and Arthur Keith:

Smith: The Piltdown Skull (October 2 ) + Keith: The Piltdown Skull and Brain Cast (October 16) + Smith. (October 30) + Keith (November 6) + Smith (November 13) + Keith (November 20). With article by Waterston disputing both.

Royal Anthropological Institute. Nature (Oct 1914)

Keith vs ASW on skull

The Significance of the Discovery at Piltdown.Bedrock: A Quarterly Journal of Scientific Thought . (1914)

Keith on Reconstruction. Nature (October 1914)

Review of Osborn Men of the Old Stone Age Man (1917)

Osborn "at sea as regards the discovery at Piltdown" because he believes skull is human but jaw chimpanzee

The Antiquity of Piltdown. Antiquity of Man (1925 ed)

Keith, Smith, Woodward, Duckworth on The Fossil Anthropoid Ape from Taugns. Nature (1925)

Revival of the Piltdown Controversy New Discoveries Relating to the Antiquity of Man (1931)

The Piltdown Man Discovery Unveiling of a Monolith Memorial Nature (1938)

Australopithecinae or Dartians. Nature (1947)

recommends "Dartian" rather than "Australopithicine" for fossil hominid

Piltdown Man: a Re-examination. Nature (1938) comment on Keith

Piltdown Recollections.An Autobiography (1950)

 

Grafton Elliot Smith

Presidential Address 1912 (September 1912)

• 1913 debate in Nature between Elliot Smith and Arthur Keith:

Smith: The Piltdown Skull (October 2 ) + Keith: The Piltdown Skull and Brain Cast (October 16) + Smith,. (October 30) + Keith, (November 6) + Smith,. (November 13) + Keith, (November 20). With article disputing both by Waterston.

The Cranial Cast of the Piltdown Skull. (September 1916)

The Problem of the Piltdown Jaw: Human or Sub-Human? (1917)

• Primitive Man The Evolution of Man (1924) + The Origin of Man

Keith, Smith, Woodward, Duckworth on The Fossil Anthropoid Ape from Taugns, (1925)

The Discovery of the Men of Heidelberg and Piltdown

The Search for Man's Ancestors (1931)

Human Palæontology (1931)

on Smith talks:

Literary and Philosophical Society (December 1913)

Royal Society, February 19 (February 1914)

Literary and Philosophical Society (March 1916)

ƒ Man of the Dawn How Our Ancestors Live. Professor Elliot Smith in Sydney

(July 1914)

The Piltdown Skull. (1922 )

Smith on new reconstruction of skull showing it aligns with cranium

 

 

 

 

 

W.J. Sollas

• Ancient Piltdown Ancient Hunters and their Modern Represenatives.. (1924 3^rd ed.)

A. G. Thacker. Science Progress in the Twentieth Century

Human Palæontology and Anthropology (1915)

Woodward. Sherborne Horse's Head. Letter to Nature   (January 1926) answered by W. J. Sollas + C. J. Bayzand. The Palæolithic Drawing of a Horse from Sherborne, Dorset + R. Elliot Steel. Drawing of a Horse from Sherborne

+ E. A. Ross Jefferson. Letter on Sherborne Horse's Head.

 Back to the
MAP

[Selkie]

Hey Danny don't even bother with Ichneumon,
I checked his info page and it *appears* his one solitary source of release in life is pontificating on FR.

Posting a million links to one's own posts is quite bemusing.

Just ignore him.


PAX :-)

[Selkie]

Do you still hold the same view that Eta Carinae's "gamma rays could cause serious (or fatal) problems on Earth" (your exact words in quotes from a while back)

Because that's not what researchers at the Chandra Observatory have to say.

[bvw]

Before I sign on to being a "YEC" wou'll have to tell me in whose hands the 24-hour clock was. Maybe it was spiralling into a black hole. That's a intellectual suggestion. btw.

[Tribune7]

[I'm not going to waste my time rebutting the entire thing, but if you'd like to point out the one or two parts you feel are most supportive of ID, I'll explain what's wrong with them.] . . . One thing for you to consider is how neo-Darwinism fails completely to account for the Cambrian explosion. . . .I'd be glad to "consider" that if you could actually make a case for such a claim. But neither Meyers article nor anything you've posted here actually supports such an assertion.

From the article:

Can neo-Darwinism explain the discontinuous increase in CSI that appears in the Cambrian explosion--either in the form of new genetic information or in the form of hierarchically organized systems of parts? We will now examine the two parts of this question . . .
In the first scenario, neo-Darwinists envision new genetic information arising from those sections of the genetic text that can presumably vary freely without consequence to the organism. . . The scenario has an overriding problem, however: the size of the combinatorial space (i.e., the number of possible amino acid sequences) and the extreme rarity and isolation of the functional sequences within that space of possibilities. Since natural selection can do nothing to help generate new functional sequences, but rather can only preserve such sequences once they have arisen, chance alone--random variation--must do the work of information generation--that is, of finding the exceedingly rare functional sequences within the set of combinatorial possibilities. Yet the probability of randomly assembling (or “finding,” in the previous sense) a functional sequence is extremely small. . . .
Other considerations imply additional improbabilities. First, new Cambrian animals would require proteins much longer than 100 residues to perform many necessary specialized functions. Ohno (1996) has noted that Cambrian animals would have required complex proteins such as lysyl oxidase in order to support their stout body structures. Lysyl oxidase molecules in extant organisms comprise over 400 amino acids. These molecules are both highly complex (non-repetitive) and functionally specified. Reasonable extrapolation from mutagenesis experiments done on shorter protein molecules suggests that the probability of producing functionally sequenced proteins of this length at random is so small as to make appeals to chance absurd, even granting the duration of the entire universe. . .
The selection/mutation mechanism faces another probabilistic obstacle. The animals that arise in the Cambrian exhibit structures that would have required many new types of cells, each of which would have required many novel proteins to perform their specialized functions. . .
Natural selection selects for functional advantage. But new cell types require whole systems of proteins to perform their distinctive functions.

Say what you want but the assertion that neo-Darwinism can't explain the Cambrian explosion, and why it can't, makes up a pretty big piece of the article. Did you read it? Did you understand it?

The third sentence -- Yet without functional criteria to guide a search through the space of possible sequences, random variation is probabilistically doomed." , however, is flat wrong.So please explain how "this is a pretty good criticism of non-design arguments".

Didn't you offer to explain what was wrong?

[furball4paws]

Holy cow!

I guess you guys don't need a microbiologist to help stir the pot.

[Ichneumon]

[1. Piltdown man : Not published in a peer-reviewed journal. Strike one]

And you have the gall to call me a liar????

Yup, when the shoe fits, I sure do. Although I didn't in this particular case -- I disagreed that this example of yours was a valid example of what you were attempting to demonstrate. If you can actually provide support for your case, I'll be glad to revise this one item to a "hit" instead of a "strike". But your following list-o-links (none of which actually *work*) doesn't qualify:

REPORTS ON THE FINDS: 1912-1917

That's sweet and all, but the formal peer-reviewed journal submission process didn't begin until around the 1950's. Before that there was sometimes informal review by a panel before publication, but it was by no means consistent or even applied at all in many cases. Any professional journal publications before 1950 or so should be considered as unreviewed, unless there is existing documentation of such a review process for a particular article's publication process. See the following, for example, which is the most cited article on the history of the modern peer-review journal publication process:

The evolution of editorial peer review.

Burnham JC.

Department of History, Ohio State University, Columbus 43210-1367.

Practically no historical accounts of the evolution of peer review exist. Biomedical journals appeared in the 19th century as personal organs, following the model of more general journalism. Journal editors viewed themselves primarily as educators. The practice of editorial peer reviewing did not become general until sometime after World War II. Contrary to common assumption, editorial peer review did not grow out of or interact with grant peer review. Editorial peer review procedures did not spread in an orderly way; they were not developed from editorial boards and passed on from journal to journal. Instead, casual referring out of articles on an individual basis may have occurred at any time, beginning in the early to mid-19th century. Institutionalization of the process, however, took place mostly in the 20th century, either to handle new problems in the numbers of articles submitted or to meet the demands for expert authority and objectivity in an increasingly specialized world.

Publication Types:

• Historical Article

PMID: 2406470 [PubMed - indexed for MEDLINE]

Now, do you have any actual documentation that any of the "complete sh!t" (as you so charmingly put it) material about "Piltdown Man" was actually peer-reviewed in the sense that it means in modern terms? Because if not, I'm still going to have to mark this one as a "strike". You asserted that, "Creationists have been seeing complete sh!t published in peer reviewed so-called scientific journals for decades". Clearly you were claiming that "complete sh!t" regularly passes the peer-review process as we know it. Clearly your example of "Piltdown Man" has yet to be substantiated by you as an actual example of what you claimed. Feel free to actually document it, or retract it. Until then, you earn a "strike" for making yet another unsubstantiated accusation against science and its institutions.

Even if you manage to pull this one out, and I don't think you can, the best you've managed is to show just two examples over 80 years apart. If the creationists were that reliable in the long run, I'd be *ecstatic*. So your broad accusation which implied a constant run of such "sh!t" for "decades" is still a falsehood.

Maybe you should actually have some sort of valid case before you shoot your mouth off with accusations again.

Now let's look at a few of your (non-working) links:

REPORTS ON THE FINDS: 1912-1917
Dawson, Woodward, and Elliot Smith, talk delivered Dec. 1912 at Geological Society on first finds

A talk is not a publication in a peer-reviewed journal. Nice try.

Woodward, Sherborne Horse's Head. et al. Letters to Nature (1926)

Letters to a journal are not peer-reviewed publications. Nice try.

The Second Piltdown Skull. letter to Nature (1933)

Letter.

Lewis Abbott This CD-ROM presents the only (though partial) anthology of Lewis Abbott publications. The Section Exposed in the Foundations of the New Admiralty Offices. (1892) Plateau Man in Kent. (1894 ) The New Oban Cave.(1895) "diminutive Forms of Flint Implements from Hastings Kitchen Midden and Sevenoaks." Worked Flints from the Cromer Forest Bed. (1897). Primeval Refuse Heaps at Hastings. 2 parts, (1897) ƒ On the Classification of the British Stone Age Industries (1911)

What in the hell are these? The Piltdown specimen was discovered in 1912. None of these pre-1912 publications could have anything whatsoever to do with it. So what are you doing here -- posting irrelevant random links in the hopes that no one will notice that you're just padding out your "case" with irrelevancies? Nice try.

Significance of Australopithecines (1953) other hominds, but no mention of Piltdown

Um, okay... See the above note about irrelevant crap in your list.

Arthur Conan Doyle: Challenger and Other Fossils. The Lost World (1912)

ROFL!!!

Let me get this straight -- as "support" for your claim that peer-reviewed science journals published "sh!t" on Piltdown Man, you're listing A NOVEL BY ARTHUR CONAN DOYLE????? Let's look at the opening paragraph, shall we?

"MR. HUNGERTON, HER FATHER, REALLY WAS THE MOST TACTless person upon earth-a fluffy, feathery, untidy cockatoo of a man, perfectly good-natured, but absolutely centered upon his own silly self. If anything could have driven me from Gladys, it would have been the thought of such a father-in-law. I am convinced that he really believed in his heart that I came round to the Chestnuts three days a week for the pleasure of his company, and very especially to hear his views on bimetallism -- a subject upon which he was by way of being an authority."

Oh, yeah, *THAT* helps your case and credibility. ROFL!!! I repeat the question I find I have to frequently ask you -- are you sure you know what in the heck you're talking about?

The "Challenger and Other Fossils" you mention in this context is not an actual reference to real *fossils*, it's a playful poke at one of the NOVEL's colorful characters, Professor Challenger, who is rather an old fossil himself.

This novel (repeat *NOVEL*), by the way, is the basis for the following cheesy TV series:

The red-bearded fellow in the pith helmet in the upper right is Professor Challenger, by the way.

*THIS* IS THE KIND OF FLUFF YOU USE TO "SUPPORT" YOUR ACCUSATION? ROFL!!!!!!!!!!!!!

Try again when you might have a clue.

[Ichneumon]

Don't leave and miss the fun -- see post #133.
And the more the merrier.

[PatrickHenry]

Thanks for posting that poster. That's something I'd like to peer review.

[Ichneumon]

Say what you want but the assertion that neo-Darwinism can't explain the Cambrian explosion, and why it can't, makes up a pretty big piece of the article.

Sure does, but Meyers arguments are fundamentally flawed. And they fail to provide anything even close to your absolute assertion that "neo-Darwinism fails completely to account for the Cambrian explosion". Even *Meyer* doesn't go so far as to make such absolute claim.

Did you read it? Did you understand it?

Absolutely. And moreoever, I know enough about the subject to spot the places where Meyer plays sleight-of-hand in order to make his case appear solid when it's not.

How about you? Do you have enough of a background to assess Meyer's assertions? Or do you just have to take them "on faith"? I suspect the latter, because everyone I know who actually *does* have a good background in these fields considers Meyer's article to be hand-waving pap.

I have to run in a few minutes to help a friend move some appliances to her new house I helped her get (hey, what was that some twit was saying about how my "one solitary source of release in life is pontificating on FR"? wrong again, kids), but I'll dissect that passage you quoted when I get back.

[Alamo-Girl]

Thank you for your reply!

The "primordial pizza" is a slang term *for* the hydrothermal vent scenario. Here you make it sound as if one has replaced the other, when in fact they are the same thing. Or have I misunderstood/missed your point here?

My point is that evidently the move to mineral clay scenarios changes the emphasis from a singular watery environment to a mixed or phased environment and that trend continues. For Lurkers:

Abiogenesis

[speaking of the Urey-Miller experiments being repeated with success] But the Earth's early atmosphere is nowadays thought to be neutral, consisting mostly of nitrogen and carbon dioxide, instead of hydrogen, ammonia, and methane (reducing), as had been suggested from cosmochemical grounds. Urey-Miller experiments performed with a neutral mixture are much less successful than those with a reducing mixture; however, the early Earth could easily have had reducing microenvironments, like hot springs and hydrothermal vents.

There is also the conundrum that bodies of water are poor places for the formation of biomolecules like proteins and nucleic acids, since the "primordial soup" is inevitably very dilute, making it difficult for molecules to "find" each other. This conundrum has led to the "primordial pizza" hypothesis of the origin of life on mineral surfaces like clay surfaces, which organic molecules can easily stick to, and which have catalytic properties that can easily assist in the formation of complex molecules. Günter Wächtershäuser has proposed that the Krebs Cycle (a.k.a. citric acid cycle, tricarboxylic acid cycle) had originated on such mineral surfaces, powered by iron-sulfur chemistry.

And while some biological molecules, like the smaller amino acids and nucleic-acid bases, are readily produced in Urey-Miller experiments, others, like sugars, are not. This means that nucleic acids are difficult to produce, since they contain the sugar ribose and its derivatives; this is a major difficulty with the otherwise-very-attractive "RNA world" hypothesis.

Thus, how to get from there to a complete self-reproducing system is still an unsolved problem, but this question is being actively researched.

Armen Y Mulkidjanian, Dmitry A Cherepanov, and Michael Y Galperin

Indeed, biochemical condensation reactions proceed with release of water, so that the presence of latter favors hydrolysis of biological polymers. Because of this feature, Bernal [27] and many researchers after him (as reviewed in ref. [10]) advanced the view that life has begun in tidal regions, so that condensation of primordial monomers proceeded under "fluctuating" conditions where the wet periods, enabling the exchange of reagents, alternated with dry ones, favoring the condensation reactions. The awareness of the potential danger of the UV damage, however, prompted other scientists to invoke a UV-protecting water layer (see e.g. ref. [19]), which apparently would impede the condensation reactions. More recently, several authors even moved the point of the life origin to the bottom of the ocean, where the reducing power of minerals and/or of hydrothermal vents was considered to be the energy source for the first condensation events [28,29]. It remained unexplained, though, how inorganic reductants could drive primordial condensation reactions in water in the absence of enzymes (see the discussion in refs. [30,31]).

In a sense, the absence of a consensus on a plausible mechanism for the origin and accumulation of the first RNA-like molecules has significantly hurt the development in the whole field and stimulated proliferation of the Panspermia hypothesis, not to mention various kinds of creationist ideas. It appears that our consideration of the UV irradiation as a positive, selective factor in primordial evolution may suggest a way out of the dead end. This view allows to place the cradle of life onto the sun-illuminated (semi) dry surface of the ancient Earth, as originally considered by Bernal [27]. Indeed, no other known energy source could compete with the UV component of the solar irradiation either in ability to serve simultaneously as both selective and driving force, or in continuity, strength, and access to the whole surface of Earth..

Multi-Phase Artificial Chemistry

The most accepted model for the origin of life has been proposed by [13,17] with the primordial ‘soup’. Hot deep sea vents as the birth place of life (the primordial ‘pizza’) were discussed as an interesting alternative [26. However, all these models need a prebiotic chemistry with complicated synthesis. As described in [20] and [21], they cannot occur in single, unpartitioned environment. A sequence of different environments would be important for the orgin of life, just as in the traditional organic synthesis. During such a synthesis a reaction mixture is subjected to certain conditions, then some products are extracted, purified, and/or crystallized, new reagents might be added, and the next step with new conditions begins. We can imagine an analogous situation in prebiotic chemistry, where the different conditions and steps are mimicked by different environments, i.e. phases like hot vents, the atmosphere, and ice, and intermittent evaporation, phase change, crystallization or filtration. This might mitigate the problems of complicated synthesis in prebiotic chemistry.

You also said wrt the fallacy of quantizing the continuum:

That wasn't the reason for the raising of the fallacy, nor were the participants in that thread "unwilling to accept" that there could be a definition of life vs non-life. The disagreement was over whether there were graduated states in between.

This particular fallacy was born at post 633 on the Plato thread. A review of the posts before and after make it very clear that the fallacy was raised due to an unwillingness of correspondents to accept there could be a definition of life v non-life/death.

At post 643, I summarized the effect of the fallacy – i.e. that it kills any investigation of abiogenesis (non-life to life) by declining to quantize either term. Prior to the fallacy, an agreement had been reached on a definition – summarized at 491, agreed at 522.

[Ichneumon]

A review of the posts before and after make it very clear that the fallacy was raised due to an unwillingness of correspondents to accept there could be a definition of life v non-life/death.

Again, I strongly disagree with that assessment. And yes, I've reviewed the posts.

At post 643, I summarized the effect of the fallacy – i.e. that it kills any investigation of abiogenesis (non-life to life) by declining to quantize either term.

And I've stated my objections to such a conclusion. Life and abiogenesis can still be analyzed and discussed, and if anything is *enhanced* by a recognition that life is not a "black or white" property, there exist "shades of gray" between "not living at all" and "life as we know it".

Again, the participants weren't "unwilling to accept" that there can be a definition of life, they were just objecting to the oversimplified "black-or-white" kind of definition which was being proposed.

Whether you agree or disagree with that particular objection, it does no good to misdescribe the actual discussion.

[Ichneumon]

Oh, what the heck... If you can post the entire Meyer article, I'll post one of the rebuttals in full. I strongly encourage Meyer's fans in the ID camp to read it in its entirety. It does an excellent job of identifying many of Meyer's misrepresentations, errors, and rhetorical sleighst-of-hand, as well as providing a glimpse of the massive amount of scientific evidence which Meyer "forgot" to acknowledge (e.g. his failure to mention gene duplication should have been grounds for bouncing his paper out of peer-review *all by itself*):

Meyer's Hopeless Monster

Posted by Wesley R. Elsberry on August 24, 2004 05:56 PM

Review of Meyer, Stephen C. 2004. The origin of biological information and the higher taxonomic categories. Proceedings of the Biological Society of Washington 117(2):213-239.

by Alan Gishlick, Nick Matzke, and Wesley R. Elsberry

[The views and statements expressed here are our own and not necessarily those of NCSE or its supporters.]

“Intelligent design” (ID) advocate Stephen C. Meyer has produced a “review article” that folds the various lines of “intelligent design” antievolutionary argumentation into one lump.  The article is published in the journal Proceedings of the Biological Society of Washington.  We congratulate ID on finally getting an article in a peer-reviewed biology journal, a mere fifteen years after the publication of the 1989 ID textbook Of Pandas and People, a textbook aimed at inserting ID into public schools.  It is gratifying to see the ID movement finally attempt to make their case to the only scientifically relevant group, professional biologists.  This is therefore the beginning (not the end) of the review process for ID.  Perhaps one day the scientific community will be convinced that ID is worthwhile.  Only through this route — convincing the scientific community, a route already taken by plate tectonics, endosymbiosis, and other revolutionary scientific ideas — can ID earn a legitimate place in textbooks. 

Unfortunately, the ID movement will likely ignore the above considerations about how scientific review actually works, and instead trumpet the paper from coast to coast as proving the scientific legitimacy of ID.  Therefore, we would like to do our part in the review process by providing a preliminary evaluation of the claims made in Meyer’s paper.  Given the scientific stakes, we may assume that Meyer, Program Director of the Discovery Institute’s Center for Science and Culture, the major organization promoting ID, has put forward the best case that ID has to offer.  Discouragingly, it appears that ID’s best case is not very good.  We cannot review every problem with Meyer’s article in this initial post, but we would like to highlight some of the most serious mistakes.  These include errors in facts and reasoning. Even more seriously, Meyer’s paper omits discussion or even citation of vast amounts of directly relevant work available in the scientific literature. 

Summary of the paper

Meyer’s paper predictably follows the same pattern that has characterized “intelligent design” since its inception: deny the sufficiency of evolutionary processes to account for life’s history and diversity, then assert that an “intelligent designer” provides a better explanation. Although ID is discussed in the concluding section of the paper, there is no positive account of “intelligent design” presented, just as in all previous work on “intelligent design”.  Just as a detective doesn’t have a case against someone without motive, means, and opportunity, ID doesn’t stand a scientific chance without some kind of model of what happened, how, and why.  Only a reasonably detailed model could provide explanatory hypotheses that can be empirically tested.  “An unknown intelligent designer did something, somewhere, somehow, for no apparent reason” is not a model.

Meyer’s paper, therefore, is almost entirely based on negative argument.  He focuses upon the Cambrian explosion as an event he thinks that evolutionary biology is unable to account for. Meyer asserts that the Cambrian explosion represented an actual sudden origin of higher taxa; that these taxa (such as phyla) are “real” and not an artifact of human retrospective classification; and that morphological disparity coincides with phyletic categories.  Meyer then argues that the origin of these phyla would require dramatic increases in biological “information,” namely new proteins and new genes (and some vaguer forms of “information” at higher levels of biological organization).  He argues that genes/proteins are highly “complex” and “specified,” and that therefore the evolutionary origin of new genes is so improbable as to be effectively impossible.  Meyer briefly considers and rejects several theories proposed within evolutionary biology that deal with macroevolutionary phenomena.  Having rejected these, Meyer argues that ID is a better alternative explanation for the emergence of new taxa in the Cambrian explosion, based solely upon an analogy between “designs” in biology and the designs of human designers observed in everyday experience.

The mistakes and omissions in Meyer’s work are many and varied, and often layered on top of each other.  Not every aspect of Meyer’s work can be addressed in this initial review, so we have chosen several of Meyer’s major claims to assess.  Among these, we will take up the Cambrian explosion and its relation to paleontology and systematics. We will examine Meyer’s negative arguments concerning evolutionary theories and the origin of biological “information” in the form of genes.

An expanded critique of this paper is in preparation.

Playing with Dynamite: The Cambrian Explosion

The Cambrian explosion is a standard topic for antievolutionists. There are several reasons for this: many taxa make their first appearance in the Cambrian explosion; the amount of time within the period of the Cambrian explosion is geologically brief; and we have limited evidence from both within and before the Cambrian explosion on which to base analysis. The first two factors form the basis of an antievolutionary argument that evolutionary processes are insufficient to generate the observed range of diversity within the limited time available. The last factor is a general feature of the sorts of phenomena that antievolutionists prefer: not enough evidence has yet accrued to single out a definitive scientific account, so it is rhetorically easy for a pseudoscientific “alternative” to be offered as a competitor. In Meyer’s closing paragraph, he mentions “experience-based analysis.”  The consistent experience of biologists is that when we have sufficient evidence bearing upon some aspect of biological origins, evolutionary theories form the basis of explanation of those phenomena (an example where much evidence has become available recently is the origin of birds and bird flight; see Gishlick 2004).

Problems with Meyer’s discussion of the Cambrian Explosion:

1. Meyer tries to evaluate morphological evolution by counting taxa, a totally meaningless endeavor for investigating the evolution of morphology. Most paleontologists gave up taxa-counting long ago and moved on to more useful realms of research regarding the Cambrian (see Budd and Jensen 2000). This is perhaps why most of Meyer’s citations for this section are to his own articles (themselves not in relevant scientific journals).

2. Meyer repeats the claim that there are no transitional fossils for the Cambrian phyla. This is a standard ploy of the Young-Earth Creationists (see Padian and Angielczyk 1999 for extended discussion of this tactic and its problems). Meyer shows a complete lack of understanding of both the fossil record and the transitional morphologies it exhibits (even during the Cambrian explosion; for a recent example of transitional forms in the Cambrian explosion see Shu et al. 2004) as well as the literature he himself cites. (This topic has been dealt with before, as with DI Fellow Jonathan Wells. See Gishlick 2002 at http://www.ncseweb.org/icons/icon2tol.html.)

3. Meyer attempts to argue that the “gaps” in the fossil record reflect an actual lack of ancestors for Cambrian phyla and subphyla.  To support this, Meyer cites some papers by University of Chicago reasearcher Mike Foote.  However, of the two papers by Foote cited by Meyer, neither deals with the Cambrian/Precambrian records (one concerns the Middle and Late Paleozoic records of crinoids and brachiopods, the other the Mesozoic record of mammal clade divergence), or even transitional fossils. Foote’s papers deal with issues of taxonomic sampling: How well does a fossil record sample for a given time period reflect the biodiversity of that period?  How well does a given fossil record pinpoint divergence times? Foote’s conclusions are that we have a good handle on past biodiversity, and that divergence times probably match appearance in the fossil record relatively closely. But Foote’s work utilizes organisms that are readily preserved.  It doesn’t deal with organisms that aren’t readily preserved, a trait that almost certainly applies to the near-microscopic, soft-bodied ancestors of the Cambrian animals.  According to Meyer’s argument, which doesn’t take into account preservation potential, microscopic metazoans such as rotifers must have arisen recently because they entirely lack a fossil record. Neither of Foote’s papers supports Meyer’s contention that the lack of transitional fossils prior to the Cambrian indicates a lack of ancestors.  Lastly, it appears that fossils of the long-hypothesized small, soft-bodied precambrian worms have recently been discovered (Chen et al. 2004).

Information and Misinformation

For some, “information theory” is simply another source of bafflegab. And that appears to be the only role Meyer sees for “information theory”. After brief nods to Shannon and algorithmic information theory, Meyer leaves the realm of established and accepted information theoretic work entirely.

1. Meyer invokes Dembski’s “specified complexity”/”complex specified information” (SC/CSI) as somehow relevant to the Cambrian explosion. However, under Dembski’s technical definition, CSI is not just the conjoint use of the nontechnical words “specified” (as in “functional”) and “complexity”, as Meyer erroneously asserts.  According to Dembski’s technical definition, improbability of appearance under natural causes is part of the *definition* of CSI.  Only after one has determined that something is wildly improbable under natural causes can one conclude that something has CSI.  You can’t just say, “boy, that sure is specific and complicated, it must have lots of CSI” and conclude that evolution is impossible.  Therefore, Meyer’s waving about of the term “CSI” as evidence against evolution is both useless for his argument, and an incorrect usage of Dembski (although Dembski himself is very inconsistent, conflating popular and technical uses of his “CSI,” which is almost certainly why Meyer made this mistake.  See here for examples of definitional inconsistency.).

2. Meyer relies on Dembski’s “specified complexity,” but even if he used it correctly (by rigorously applying Dembski’s filter, criteria, and probability calculations), Dembski’s filter has never been demonstrated to be able to distinguish anything in the biological realm — it has never been successfully applied by anyone to any biological phenomena (Elsberry and Shallit, 2003).

3. Meyer claims, “The Cambrian explosion represents a remarkable jump in the specified complexity or ‘complex specified information’ (CSI) of the biological world.” Yet to substantiate this, Meyer would have to yield up the details of the application of Dembski’s “generic chance elimination argument” to this event, which he does not do. There’s small wonder in that, for the total number of attempted uses of Dembski’s CSI in any even partially rigorous way number a meager four (Elsberry and Shallit, 2003).

4. Meyer claims, “One way to estimate the amount of new CSI that appeared with the Cambrian animals is to count the number of new cell types that emerged with them (Valentine 1995:91-93)” (p.217). This may be an estimate of something, and at least signals some sort of quantitative approach, but we may be certain that the quantity found has nothing to do with Dembski’s CSI. The quantitative element of Dembski’s CSI is an estimate of the probability of appearance (under natural processes or random assembly, as Dembski shifts background assumptions opportunistically), and has nothing to do with counting numbers of cell types.

Of Text and Peptides

1. Meyer argues that “many scientists and mathematicians have questioned the ability of mutation and selection to generate information in the form of novel genes and proteins” (p. 218).  He makes statements to this effect throughout the paper.  Meyer does not say who these scientists are, and in particular does not say whether or not any of them are biologists.  The origin of new genes and proteins is actually a common, fairly trivial event, well-known to anyone who spends a modicum of effort investigating the scientific literature.  The evolution of new genes has been observed in the lab, in the wild, inferred in great detail between closely-related modern species, and reconstructed in hundreds of cases by comparing the genomes from organisms sequenced in genome projects over the last decade (see Long 2001 and related articles, and below).

2. Meyer compares DNA sequences to human language.  In this he follows Denton’s (1986) Evolution: A Theory in Crisis.  Denton (1986) argued that meaningful sentences are isolated from each other: it is usually impossible to convert one sentence to another via a series of random letter changes, where each intermediate sentence has meaning. Like Denton (1986), Meyer applies the same argument to gene and protein sequences, concluding that they, like meaningful sentences, must have been produced by intelligent agents.  The analogy between language and biological sequence is poor for many reasons; starting with the most obvious point of disanalogy, proteins can lose 80% or more of their sequence similarity and retain the same structure and function (a random example is here). Let’s examine an English phrase where four out of five characters have been replaced with a randomly generated text string.  See if you can determine the original meaning of this text string:

Tnbpursutd euckilecuitn tiioismdeetneia niophvlgorciizooltccilhseema er [1]

Eighty percent loss of sequence identity is fatal to English sentences. Clearly proteins are much less specified than language.

3. Meyer cites Denton (1986) unhesitatingly.  This is surprising because, while Denton advocated in 1986 that biology adopt a typological view of life, he has abandoned this view (Denton 1998).  Among other things, Denton wrote, “One of the most surprising discoveries which has arisen from DNA sequencing has been the remarkable finding that the genomes of all organisms are clustered very close together in a tiny region of DNA sequence space forming a tree of related sequences that can all be interconverted via a series of tiny incremental natural steps.” (p. 276)  Denton now accepts common descent and disagrees with the “intelligent design” advocates who conjecture the special creation of biological groups, regularly criticizing them for ignoring the overwhelming evidence (Denton 1999).

4. Meyer’s case that the evolution of new genes and proteins is essentially impossible relies on just a few references from the scientific literature. For example, Meyer references Taylor et al. 2001, a paper entitled “Searching sequence space for protein catalysts” and available online at the PNAS website.  But Taylor et al.’s recommendation for intelligent protein design is actually that it should mimic natural evolution: “[A]s in natural evolution, the design of new enzymes will require incremental strategies…”.

There is a large mass of evidence supporting the view that proteins are far less “specified” than Meyer asserts.  Fully reviewing this would require an article in itself, and would be somewhat beside the point since Meyer’s claim is categorically disproven by the recent origin of novel genes by natural processes.  (Another way in which “experience-based analysis” leads one to conclusions other than those Meyer asserts.) However, some idea of the diversity of protein solutions to any given enzymatic “problem” is given at the NCBI’s Analogous Enzymes webpage, which includes hundreds of examples.  There is more than one way to skin a cat, and there are many more ways to evolve a solution to any given functional “problem” in biology.

The origin of novel genes/proteins

Meyer makes his case that evolution can’t produce new genes in complete neglect of the relevant scientific literature documenting the origin of new genes. 

1. A central claim of Meyer’s is that novel genes have too much “CSI” to be produced by evolution. The first problem with this is that Meyer does not demonstrate that genes have CSI under Dembski’s definition (see above). The second problem is that Meyer cites absolutely none of the literature documenting the origin of new genes.  For example, Meyer missed the recent paper in Current Opinion in Genetics and Development with the unambiguous title, “Evolution of novel genes.” The paper and 183 related papers can be found here.  Many other references can be found linked from here.

It is worth listing a few in-text to make crystal-clear the kinds of references that Meyer missed:

Copley, S. D. (2000). “Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach.” Trends Biochem Sci 25(6): 261-265. PubMed

Harding, M. M., Anderberg, P. I. and Haymet, A. D. (2003). “‘Antifreeze’ glycoproteins from polar fish.” Eur J Biochem 270(7): 1381-1392. PubMed

Johnson, G. R., Jain, R. K. and Spain, J. C. (2002). “Origins of the 2,4-dinitrotoluene pathway.” J Bacteriol 184(15): 4219-4232. PubMed

Long, M., Betran, E., Thornton, K. and Wang, W. (2003). “The origin of new genes: glimpses from the young and old.” Nat Rev Genet 4(11): 865-875. PubMed

Nurminsky, D., Aguiar, D. D., Bustamante, C. D. and Hartl, D. L. (2001). “Chromosomal effects of rapid gene evolution in Drosophila melanogaster.” Science 291(5501): 128-130. PubMed

Patthy, L. (2003). “Modular assembly of genes and the evolution of new functions.” Genetica 118(2-3): 217-231. PubMed

Prijambada I. D., Negoro S., Yomo T., Urabe I. (1995). “Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution.” Appl Environ Microbiol. 61(5):2020-2. PubMed

Ranz, J. M., Ponce, A. R., Hartl, D. L. and Nurminsky, D. (2003). “Origin and evolution of a new gene expressed in the Drosophila sperm axoneme.” Genetica 118(2-3): 233-244. PubMed

Seffernick, J. L. and Wackett, L. P. (2001). “Rapid evolution of bacterial catabolic enzymes: a case study with atrazine chlorohydrolase.” Biochemistry 40(43): 12747-12753. PubMed

2. Meyer cites Axe (2000) as a counter to the evolutionary scenario of successive modifications of genes leading to new protein products. But Axe (2000) is not in any sense about “successive modifications”; Axe modified proteins in several locations at a time.  ID advocates love to cite certain Axe papers that indicate that functional proteins are rare in sequence space, but not others that indicate the opposite (Axe et al., 1996).  Axe apparently said in 1999 that his work had no relevance to intelligent design.

3. Meyer portrays protein function as all-or-nothing. But protein function is not all-or-nothing. Recent research highlights several evolutionary mechanisms “tinkering” with existing genes to arrive at new genes (Prijambada et al. 1995; Long 2001). But you won’t learn about that from Meyer.

4. As far as we can tell, Meyer uses the word “duplication” or something similar only twice in the entire 26-page article.  One of these usages is in the references, in the title of an article referring to centriole duplication.  The other is on p. 217, where Meyer introduces the genes-from-unnecessary DNA scenario. However, he subsequently ignores duplicated functional genes in this section and focuses on the origin of genes from noncoding DNA. Duplication really belongs with Meyer’s section on the second evolutionary scenario, the origin of genes from coding DNA.  There, Meyer argued that the origin of new genes from old genes was impossible because such a process would mess up the function of the old genes.  If he had put it there, he would have revealed the existence of the extremely simple, and already well-known, solution to the problem that he posed, namely, gene duplication (Lynch and Conery, 2000, 2003).

5. Meyer relies heavily on a new paper by Axe published in the Journal of Molecular Biology. Meyer alleges that Axe (2004) proves that, “the probability of finding a functional protein among the possible amino acid sequences corresponding to a 150-residue protein is similarly 1 in 10^77.” But Axe’s actual conclusion is that the number is “in the range of one in 10^77 to one in 10^53” (Axe 2004, p. 16). Meyer only reports the lowest extreme. One in 10^53 is still a small number, but Meyer apparently didn’t feel comfortable mentioning those 24 orders of magnitude to his reader.  A full discussion of Axe (2004) will have to appear elsewhere, but it is worth noting that Axe himself discusses at length the fact that the results one gets in estimating the density of functional sequences depend heavily on methods and assumptions.  Axe uses a fairly restricted “target” in his study, which gives a low number, but studies that just take random sequences and assay them just for function — which Meyer repeatedly insists is all that matters in biology — produce larger numbers (Axe 2004, pp. 1-2). [2]

We would like to pose a challenge to Meyer.  There are a large number of documented cases of the evolutionary origin of new genes (again, a sample is here).  We challenge Meyer to explain why he didn’t include them, or anything like them, in his review.  We invite readers to wait to see whether or not Meyer ever addresses them at a later date and whether he can bring himself to admit that his most common, most frequent, and most central assertion in his paper is wildly incorrect and widely known to be so in the scientific literature.  These points should not be controversial: even Michael Behe, the leading IDist and author of Darwin’s Black Box, admits that novel genes can evolve: “Antibiotics and pesticide resistance, antifreeze proteins in fish and plants, and more may indeed be explained by a Darwinian mechanism.” (Behe 2004, p. 356)

If we might be permitted a prediction, Meyer or his defenders will respond not by admitting their error on this point, but by engaging in calculated obfuscation over the definition of the words “novel” and “fundamentally.”  They will then assert that, after all, yes, evolution can produce new genes and new information, but not “fundamentally new genes.”  They will never clarify what exactly counts as fundamental novelty.

Morphological novelty

The origin of morphological novelty is also a large topic with an extensive literature, but unfortunately we can only discuss a limited number of topics in any depth here.  To pick two issues, Meyer fails to incorporate any of the work on the origin of morphological novelties in geologically recent cases where evidence is fairly abundant, and Meyer also fails to discuss the crucial role that cooption plays in the origin of novelty.  Below is a small sampling of the kinds of papers that Meyer would have had to address in this field in order to even begin to make a case that evolution cannot produce new morphologies:

Ganfornina M. D., Sanchez D. 1999. “Generation of evolutionary novelty by functional shift.” Bioessays. 21(5):432-9. PubMed

Mayr, E. 1960. “The Emergence of Evolutionary Novelties.”  in Evolution After Darwin: Volume 1: The Evolution of Life: Its Origin, History, and Future, Sol Tax, ed.  The University of Chicago Press, Chicago, IL. pp. 349-380.

Pellmyr, O. and Krenn, H. W., 2002. “Origin of a complex key innovation in an obligate insect-plant mutualism.” PNAS. 99(8):5498-5502. PubMed

Prum, R. O. and Brush, A. H., 2002. “The evolutionary origin and diversification of feathers.” Q Rev Biol. 77 (3), 261-295. PubMed

True, J. R. and Carroll, S. B., 2002. “Gene co-option in physiological and morphological evolution.” Annu Rev Cell Dev Biol. 18, 53-80. PubMed

Mayr’s paper in particular is a well-known introduction to the topic.  He emphasized the important role of change-of-function for understanding the origin of new structures.  In his conclusion he wrote,

“The emergence of new structures is normally due to the acquisition of a new function by an existing structure.  In both cases the resulting ‘new’ structure is merely a modification of a preceding structure.  The selection pressure in favor of the structural modification is greatly increased by a shift into a new ecological niche, by the acquisition of a new habit, or by both.  A shift in function exposes the fully formed ‘preadapted’ structure to the new selection pressure.  This, in most cases, explains how an incipient structure could be favored by natural selection before reaching a size and elaboration where it would be advantageous for a new role.” (p. 377-378)

Mayr wrote this in 1960, at the sprightly age of 56, but it applies rather well to discoveries about the origin of new genes and new morphological structures made in the last few decades.  Most new genes and new structures are derived by change-of-function from old genes and old structures, often after duplication.  Many other terms are used in the evolutionary literature for this process (Mayr’s “preadaptation”, replaced by “exaptation” by Gould; cooption; functional shift; tinkering; bricolage; see e.g. the commonly-cited essay by Jacob 1977 for a discussion of the “tinkering” analogy for evolution), but none of them appear in Meyer’s essay. 

The Power of Negative Thinking

Negative argumentation against evolutionary theories seems to be the sole scientific content of “intelligent design”. That observation continues to hold true for this paper by Meyer.

1. Meyer gives no support for his assertion that PE proponents proposed species selection to account for “large morphological jumps”. (Use of the singular, “punctuated equilibrium”, is a common feature of antievolution writing. It is relatively less common among evolutionary biologists, who utilize the plural form, “punctuated equilibria”, as it was introduced by Eldredge and Gould in 1972.)

2. Meyer makes the false claim that PE was supposed to address the problem of the origin of biological information or form. As Gould and Eldredge 1977 noted, PE is a theory about speciation.  It is an application of Ernst Mayr’s theory of allopatric speciation — a theory at the core of the Modern Synthesis — to the fossil record.  Any discussion of PE that doesn’t mention allopatric speciation or something similar is ignoring the concept’s original meaning.

3. Meyer also makes the false claim that PE was supposed to address the origin of taxa higher than species. This class of error was specifically addressed in Gould and Eldredge 1977.  PE is about the pattern of speciation observed in the fossil record, not about taxa other than species.

4. Meyer makes the false claim that genetic algorithms require a “target sequence” to work. Meyer cites two of his own articles as the relevant authority in this matter. However, when one examines these sources, one finds that what is cited in both of these earlier essays is a block of three paragraphs, the content of which is almost identical in the two essays. Meyer bases his denunciation of genetic algorithms as a field upon a superficial examination of two cases. While some genetic algorithm simulations for pedagogy do incorporate a “target sequence”, it is utterly false to say that all genetic algorithms do so. Meyer was in attendance at the NTSE in 1997 when one of us [WRE] brought up a genetic algorithm to solve the Traveling Salesman Problem, which was an example where no “target sequence” was available.  Whole fields of evolutionary computation are completely overlooked by Meyer. Two citations relevant to Meyer’s claims are Chellapilla and Fogel (2001) and Stanley and Miikkulainen (2002). (That Meyer overlooks Chelapilla and Fogel 2001 is even more baffling given that Dembski 2002 discussed the work.) Bibliographies for the entirely neglected fields of artificial life and genetic programming are available at these sites:

http://users.ox.ac.uk/~econec/alife.html
http://www.cs.bham.ac.uk/~wbl/biblio/gp-bibliography.html.

A bibliography of genetic algorithms and artificial neural networks is available here.

On the Other Hand: the View Meyer Fails to Consider

When Meyer states that a massive increase in information is required to create all the body plans of the living “phyla” he is implying that evolution had to go from a single celled creature to a complex metazoan in one step, which would be impossible. But the origin of metazoans is not a case of zero to metazoan instantly. Rather, it involves a series of incremental morphological steps.  These steps become apparent when the evolution of the major clades of metazoan life is viewed in a phylogenetic context. The literature using this phylogenetic perspective is extensive if Meyer wanted to investigate it (for example see Grande and Rieppel eds. 1994, Carroll 1997, Harvey et al. eds. 1996). Certainly an acknowledgment of such literature is crucial if one is going to discuss these topics in a scholarly article, even if it was to criticize it. No discussion of an evolutionary innovation would be complete without reference to the phylogeny, and yet we find not one in Meyer’s 26 page opus.

Perhaps the glaring absence of phylogenies owes to Meyer’s lack of acceptance of common descent, or perhaps it is because when the relationships of the ‘phyla’ are seen in a phylogenetic context, one readily sees that all of the complex developmental and morphological features that diagnose the extant clades need not arise simultaneously. Rather, they are added incrementally. First one cell type, then three, multiple body layers, and bilateral symmetry. At this point you have a “worm” and all the other bauplans are basically variations on the worm theme. There are worms with guts, and worms with muscles, worms with segments, worms with appendages, and even worms with a stiff tube in them (this last would be us).

Missing from Meyer’s picture is any actual discussion of the origins of metazoan development. Reading Meyer, one would think that it is a giant mystery, but the real mystery is why Meyer does not reference this huge area of research.

Meyer implies that the lack of specificity of development in genes is a surprising problem for evolution, yet it is well known and it is widely recognized that development is coordinated by epigenetic interactions of various cell lineages. Meyer treats this fact as if it were some mysterious phenomenon requiring a designer to input information. But, just as the ordered structure of convection cells in is boiling pot of water is not a mystery to physicists even though it is not specified by the shapes of the component water molecules, neither are developmental programs to biologists. The convection cells are an emergent property of the interactions of the water molecules, just as the growth of organismal form is an emergent property of the interactions of cell lineages.

It is thought that metazoan development arose by competition between variant cell lineages that arose during ontogeny, and thus its organization remains in the epigenetic interactions of the various cell lineages (Buss 1987). This was extensively documented by Leo Buss in 1987, but Meyer somehow failed to mention this seminal work on the origin of metazoan development.

Understanding the interactions of lineages and their various reciprocal inductions is crucial to understanding the evolution of metazoan development and bodyplans. The study of this forms the basis for the entire field of evolutionary and developmental biology, Meyer acts like this field doesn’t even exist, while citing sparingly from some of its works. Also absent is any discussion of the difference between sorting and selection (see Vrba and Gould 1986). The difference is crucial: sorting at one level does not imply selection, but rather may be the result of selection at an entirely different level of the organismal hierarchy.  Meyer appears to be completely unaware of this distinction when criticizing the inability of selection to create new morphologies. In some cases novelty at one level in the hierarchy may result when selection occurs somewhere else in the hierearchy: the emergent morphology may actually be the result of a sorting cascade, rather than direct selection. The evolution of metazoan bodyplans involved an exchange between selection at the level of the individual and at the level of the cell lineage, which was sorted through developmental interactions (Buss 1987) .

Finally, any discussion of development and evolution would not be complete without dealing with the effects of heterochrony on form, and here too we find relevant citations glaringly absent despite the prominent place of heterochrony in the literature going back to de Beer. This is 60 years of research missed by Meyer. (The oversight is worse when one considers various contributing ideas in development that date back to von Baer.)

Meyer repeatedly appeals to the notion of an ur-cell metazoan ancestor that had all the genetic potentiality of the different metazoan bauplanes. The reference to this hypothetical super-ancestor is as popular with creationists as it is erroneous to biologists. While biologists have at times proposed a need for such an ur-cell, this is no longer particularly in vogue, because the recognition of hierarchy and epigenetic processes and has removed the need for an all-encompassing ancestor.

There are many hierarchies that need to be separated. There is the phylogenetic hierarchy (the order of character acquisition in time), the developmental hierarchy (the order of cell differentiation) and the structural hierarchy (the position of various parts in an organism). Meyer muddles all of these together and treats them like they are all the same thing, but they are not. 

A Long Walk Off a Short Peer Review

The Proceedings of the Biological Society of Washington (PBSW) is a respected, if somewhat obscure, biological journal specializing in papers of a systematic and taxonomic nature, such as the description of new species. A review of issues in evolutionary theory is decidedly not its typical fare, even disregarding the creationist nature of Meyer’s paper. The fact that the paper is both out of the journal’s typical sphere of publication, as well as dismal scientifically, raises the question of how it made it past peer review. The answer probably lies in the editor, Richard von Sternberg. Sternberg happens to be a creationist and ID fellow traveler who is on the editorial board of the Baraminology Study Group at Bryan College in Tennessee. (The BSG is a research group devoted to the determination of the created kinds of Genesis. We are NOT making this up!) Sternberg was also a signatory of the Discovery Institute’s “100 Scientists Who Doubt Darwinism” statement. [3] Given R. v. Sternberg’s creationist leanings, it seems plausible to surmise that the paper received some editorial shepherding through the peer review process. Given the abysmal quality of the science surrounding both information theory and the Cambrian explosion, it seems unlikely that it received review by experts in those fields. One wonders if the paper saw peer review at all.

Although this critique has focused on the scientific problems with Meyer’s paper, it may be worth briefly considering the political dimensions, as the paper is likely to become part of the ID creationists’ lobbying machine.  The paper has been out since early August, so it is somewhat puzzling that the Discovery Institute and similar groups have yet to publicize this major event for ID theory. Are they embarrassed at its sub-par (even by ID standards) content, or are they are waiting to spring it on some unsuspecting scientist at a future school board meeting or state legislature hearing?  Regardless, once the press releases start to fly, responses to the paper should be careful to not assume facts not in evidence (such as the review, or lack thereof, of Meyer’s paper), and should be careful to distinguish between issues that are scientifically important and unimportant.  Whether or not editorial discretion was abused in order to enable “intelligent design” to make a coveted appearance in the peer-reviewed scientific literature is not currently known, and is at any rate not the most important issue. The important issue is whether or not the paper makes any scientific contribution: does it propose a positive explanatory model?  If the paper is primarily negative critique, does it accurately review the science it purports to criticize?  The fact that a paper is shaky on these grounds is much more important than the personalities involved.  Intemperate responses will only play into the hands of creationists, who might use these as an excuse to say that the “dogmatic Darwinian thought police” are unfairly giving Meyer and PBSW a hard time.  Nor should Sternberg be given the chance to become a “martyr for the cause.”  Any communication with PBSW should focus upon the features that make this paper a poor choice for publication: its many errors of fact, its glaring omissions of relevant material, and its misrepresentations of the views that it does consider.

The ultimate test of the value of a peer-reviewed paper is whether it spawns actual research and convinces skeptics. Applicability and acceptance in science, not in politics, is the ultimate test of proposed scientific ideas. As we have stated before, all ID advocates have to do is demonstrate to scientists that they have something that works. They need a positive research program showing scientists that ID has more to offer than “Poof, ID did it.”

Conclusion

There is nothing wrong with challenging conventional wisdom — continuing challenge is a core feature of science.  But challengers should at least be aware of, read, cite, and specifically rebut the actual data that supports conventional wisdom, not merely construct a rhetorical edifice out of omission of relevant facts, selective quoting, bad analogies, knocking down strawmen, and tendentious interpretations.  Unless and until the “intelligent design” movement does this, they are not seriously in the game. They’re not even playing the same sport.

Postscript

As we have said, the errors in this paper are too numerous to document more than a few here.  We invite readers to find more mistakes and misrepresentations in this work and add them to our comments section, and/or email them to us to add to the full online critique.

Endnotes

1. The original phrase was: “The origin of biological information and the higher taxonomic categories”, the title of Meyer’s paper.  The random text was generated at the random text generator webpage: http://barnyard.syr.edu/monkey.html…

2. Page numbers for Axe (2004) in this section refer to the in press, pre-publication version of Axe’s paper availabe on the JMB website: http://dx.doi.org/10.1016/j.jmb.2004.06.058.

3. As mentioned previously, Meyer is the directory the Discovery Institute’s Center for Science and Culture. Meyer’s reported affiliation on the PBSW paper is to Palm Beach Atlantic University, which requires all faculty to affirm the following statement:

To assure the perpetuation of these basic concepts of its founders, it is resolved that all those who become associated with Palm Beach Atlantic as trustees, officers, members of the faculty or of the staff, must believe that man was directly created by God.

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[Alamo-Girl]

Thanks for your reply!

Again, the participants weren't "unwilling to accept" that there can be a definition of life, they were just objecting to the oversimplified "black-or-white" kind of definition which was being proposed.

Whether you agree or disagree with that particular objection, it does no good to misdescribe the actual discussion.

I leave it to the Lurkers to decide whether or not I have "misdescribed" the actual discussion.

If there can be an agreement among the correspondents as to the starting point (non-life) and the ending point (life) - then the Freeper investigation can be resumed - until then, abiogenesis is a moving target, and the Freeper research project remains dead-in-the-water.

Likewise, until a definition of life v non-life/death is ascertained - I assert that all theories of abiogenesis will not be taken seriously.