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

Stephen C. Meyer Article: The = Origin of=20 Biological Information and the Higher Taxonomic = Categories
By: Stephen=20 C. Meyer
Proceedings of the = Biological=20 Society of Washington
January 26,=20 2005

On August = 4th, 2004 an=20 extensive review essay by Dr. Stephen C. Meyer, Director of Discovery=20 Institute's Center for Science & Culture appeared in the = Proceedings of=20 the Biological Society of Washington (volume 117, no. 2, pp. = 213-239). The=20 Proceedings is a peer-reviewed biology journal published at the = National=20 Museum of Natural History at the Smithsonian Institution in Washington = D.C.=20

In the article, entitled =93The Origin of Biological Information = and the=20 Higher Taxonomic Categories=94, Dr. Meyer argues that no current = materialistic=20 theory of evolution can account for the origin of the information = necessary to=20 build novel animal forms. He proposes intelligent design as an = alternative=20 explanation for the origin of biological information and the higher = taxa.=20

Due to an unusual number of inquiries about the article, Dr. = Meyer, the=20 copyright holder, has decided to make the article available now in HTML = format=20 on this website. (Off prints are also available from Discovery Institute = by=20 writing to Keith Pennock at Kpennock@discovery.org. Please provide your = mailing=20 address and we will dispatch a copy).

PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF=20 WASHINGTON
117(2):213-239. 2004

The origin of = biological=20 information and the higher taxonomic categories
Stephen=20 C. Meyer

Introduction

In a recent volume of = the=20 Vienna Series in a Theoretical Biology (2003), Gerd B. Muller and Stuart = Newman=20 argue that what they call the =93origination of organismal form=94 = remains an=20 unsolved problem. In making this claim, Muller and Newman (2003:3-10)=20 distinguish two distinct issues, namely, (1) the causes of form = generation in=20 the individual organism during embryological development and (2) the = causes=20 responsible for the production of novel organismal forms in the first = place=20 during the history of life. To distinguish the latter case (phylogeny) = from the=20 former (ontogeny), Muller and Newman use the term =93origination=94 to = designate the=20 causal processes by which biological form first arose during the = evolution of=20 life. They insist that =93the molecular mechanisms that bring about = biological=20 form in modern day embryos should not be confused=94 with the causes = responsible=20 for the origin (or =93origination=94) of novel biological forms during = the history=20 of life (p.3). They further argue that we know more about the causes of=20 ontogenesis, due to advances in molecular biology, molecular genetics = and=20 developmental biology, than we do about the causes of phylogenesis--the = ultimate=20 origination of new biological forms during the remote past.

In = making=20 this claim, Muller and Newman are careful to affirm that evolutionary = biology=20 has succeeded in explaining how preexisting forms diversify under the = twin=20 influences of natural selection and variation of genetic traits. = Sophisticated=20 mathematically-based models of population genetics have proven adequate = for=20 mapping and understanding quantitative variability and populational = changes in=20 organisms. Yet Muller and Newman insist that population genetics, and = thus=20 evolutionary biology, has not identified a specifically causal = explanation for=20 the origin of true morphological novelty during the history of life. = Central to=20 their concern is what they see as the inadequacy of the variation of = genetic=20 traits as a source of new form and structure. They note, following = Darwin=20 himself, that the sources of new form and structure must precede the = action of=20 natural selection (2003:3)--that selection must act on what already = exists. Yet,=20 in their view, the =93genocentricity=94 and =93incrementalism=94 of the = neo-Darwinian=20 mechanism has meant that an adequate source of new form and structure = has yet to=20 be identified by theoretical biologists. Instead, Muller and Newman see = the need=20 to identify epigenetic sources of morphological innovation during the = evolution=20 of life. In the meantime, however, they insist neo-Darwinism lacks any = =93theory=20 of the generative=94 (p. 7).

As it happens, Muller and Newman are = not alone=20 in this judgment. In the last decade or so a host of scientific essays = and books=20 have questioned the efficacy of selection and mutation as a mechanism = for=20 generating morphological novelty, as even a brief literature survey will = establish. Thomson (1992:107) expressed doubt that large-scale = morphological=20 changes could accumulate via minor phenotypic changes at the population = genetic=20 level. Miklos (1993:29) argued that neo-Darwinism fails to provide a = mechanism=20 that can produce large-scale innovations in form and complexity. Gilbert = et al.=20 (1996) attempted to develop a new theory of evolutionary mechanisms to=20 supplement classical neo-Darwinism, which, they argued, could not = adequately=20 explain macroevolution. As they put it in a memorable summary of the = situation:=20 =93starting in the 1970s, many biologists began questioning its = (neo-Darwinism's)=20 adequacy in explaining evolution. Genetics might be adequate for = explaining=20 microevolution, but microevolutionary changes in gene frequency were not = seen as=20 able to turn a reptile into a mammal or to convert a fish into an = amphibian.=20 Microevolution looks at adaptations that concern the survival of the = fittest,=20 not the arrival of the fittest. As Goodwin (1995) points out, 'the = origin of=20 species--Darwin's problem--remains unsolved'=93 (p. 361). Though Gilbert = et al.=20 (1996) attempted to solve the problem of the origin of form by proposing = a=20 greater role for developmental genetics within an otherwise = neo-Darwinian=20 framework,¹=20 numerous recent authors have continued to raise questions about the = adequacy of=20 that framework itself or about the problem of the origination of form = generally=20 (Webster & Goodwin 1996; Shubin & Marshall 2000; Erwin 2000; = Conway=20 Morris 2000, 2003b; Carroll 2000; Wagner 2001; Becker & Lonnig 2001; = Stadler=20 et al. 2001; Lonnig & Saedler 2002; Wagner & Stadler 2003; = Valentine=20 2004:189-194).

What lies behind this skepticism? Is it warranted? = Is a=20 new and specifically causal theory needed to explain the origination of=20 biological form?

This review will address these questions. It = will do so=20 by analyzing the problem of the origination of organismal form (and the=20 corresponding emergence of higher taxa) from a particular theoretical=20 standpoint. Specifically, it will treat the problem of the origination = of the=20 higher taxonomic groups as a manifestation of a deeper problem, namely, = the=20 problem of the origin of the information (whether genetic or epigenetic) = that,=20 as it will be argued, is necessary to generate morphological = novelty.

In=20 order to perform this analysis, and to make it relevant and tractable to = systematists and paleontologists, this paper will examine a paradigmatic = example=20 of the origin of biological form and information during the history of = life: the=20 Cambrian explosion. During the Cambrian, many novel animal forms and = body plans=20 (representing new phyla, subphyla and classes) arose in a geologically = brief=20 period of time. The following information-based analysis of the Cambrian = explosion will support the claim of recent authors such as Muller and = Newman=20 that the mechanism of selection and genetic mutation does not constitute = an=20 adequate causal explanation of the origination of biological form in the = higher=20 taxonomic groups. It will also suggest the need to explore other = possible causal=20 factors for the origin of form and information during the evolution of = life and=20 will examine some other possibilities that have been = proposed.

The=20 Cambrian Explosion

The =93Cambrian explosion=94 refers to the = geologically sudden appearance of many new animal body plans about 530 = million=20 years ago. At this time, at least nineteen, and perhaps as many as = thirty-five=20 phyla of forty total (Meyer et al. 2003), made their first appearance on = earth=20 within a narrow five- to ten-million-year window of geologic time = (Bowring et=20 al. 1993, 1998a:1, 1998b:40; Kerr 1993; Monastersky 1993; Aris-Brosou = & Yang=20 2003). Many new subphyla, between 32 and 48 of 56 total (Meyer et al. = 2003), and=20 classes of animals also arose at this time with representatives of these = new=20 higher taxa manifesting significant morphological innovations. The = Cambrian=20 explosion thus marked a major episode of morphogenesis in which many new = and=20 disparate organismal forms arose in a geologically brief period of=20 time.

To say that the fauna of the Cambrian period appeared in a=20 geologically sudden manner also implies the absence of clear = transitional=20 intermediate forms connecting Cambrian animals with simpler pre-Cambrian = forms.=20 And, indeed, in almost all cases, the Cambrian animals have no clear=20 morphological antecedents in earlier Vendian or Precambrian fauna = (Miklos 1993,=20 Erwin et al. 1997:132, Steiner & Reitner 2001, Conway Morris = 2003b:510,=20 Valentine et al. 2003:519-520). Further, several recent discoveries and = analyses=20 suggest that these morphological gaps may not be merely an artifact of=20 incomplete sampling of the fossil record (Foote 1997, Foote et al. 1999, = Benton=20 & Ayala 2003, Meyer et al. 2003), suggesting that the fossil record = is at=20 least approximately reliable (Conway Morris 2003b:505).

As a = result,=20 debate now exists about the extent to which this pattern of evidence = comports=20 with a strictly monophyletic view of evolution (Conway Morris 1998a, = 2003a,=20 2003b:510; Willmer 1990, 2003). Further, among those who accept a = monophyletic=20 view of the history of life, debate exists about whether to privilege = fossil or=20 molecular data and analyses. Those who think the fossil data provide a = more=20 reliable picture of the origin of the Metazoan tend to think these = animals arose=20 relatively quickly--that the Cambrian explosion had a =93short fuse.=94 = (Conway=20 Morris 2003b:505-506, Valentine & Jablonski 2003). Some (Wray et al. = 1996),=20 but not all (Ayala et al. 1998), who think that molecular phylogenies = establish=20 reliable divergence times from pre-Cambrian ancestors think that the = Cambrian=20 animals evolved over a very long period of time--that the Cambrian = explosion had=20 a =93long fuse.=94 This review will not address these questions of = historical=20 pattern. Instead, it will analyze whether the neo-Darwinian process of = mutation=20 and selection, or other processes of evolutionary change, can generate = the form=20 and information necessary to produce the animals that arise in the = Cambrian.=20 This analysis will, for the most part, ²=20 therefore, not depend upon assumptions of either a long or short fuse = for the=20 Cambrian explosion, or upon a monophyletic or polyphyletic view of the = early=20 history of life.

Defining Biological Form and=20 Information

Form, like life itself, is easy to recognize but = often=20 hard to define precisely. Yet, a reasonable working definition of form = will=20 suffice for our present purposes. Form can be defined as the = four-dimensional=20 topological relations of anatomical parts. This means that one can = understand=20 form as a unified arrangement of body parts or material components in a = distinct=20 shape or pattern (topology)--one that exists in three spatial dimensions = and=20 which arises in time during ontogeny.

Insofar as any particular=20 biological form constitutes something like a distinct arrangement of = constituent=20 body parts, form can be seen as arising from constraints that limit the = possible=20 arrangements of matter. Specifically, organismal form arises (both in = phylogeny=20 and ontogeny) as possible arrangements of material parts are constrained = to=20 establish a specific or particular arrangement with an identifiable = three=20 dimensional topography--one that we would recognize as a particular = protein,=20 cell type, organ, body plan or organism. A particular =93form,=94 = therefore,=20 represents a highly specific and constrained arrangement of material = components=20 (among a much larger set of possible arrangements). =

Understanding form=20 in this way suggests a connection to the notion of information in its = most=20 theoretically general sense. When Shannon (1948) first developed a = mathematical=20 theory of information he equated the amount of information transmitted = with the=20 amount of uncertainty reduced or eliminated in a series of symbols or=20 characters. Information, in Shannon's theory, is thus imparted as some = options=20 are excluded and others are actualized. The greater the number of = options=20 excluded, the greater the amount of information conveyed. Further, = constraining=20 a set of possible material arrangements by whatever process or means = involves=20 excluding some options and actualizing others. Thus, to constrain a set = of=20 possible material states is to generate information in Shannon's sense. = It=20 follows that the constraints that produce biological form also imparted=20 information. Or conversely, one might say that producing = organismal form=20 by definition requires the generation of information.

In = classical=20 Shannon information theory, the amount of information in a system is = also=20 inversely related to the probability of the arrangement of constituents = in a=20 system or the characters along a communication channel (Shannon 1948). = The more=20 improbable (or complex) the arrangement, the more Shannon information, = or=20 information-carrying capacity, a string or system = possesses.

Since the=20 1960s, mathematical biologists have realized that Shannon's theory could = be=20 applied to the analysis of DNA and proteins to measure the = information-carrying=20 capacity of these macromolecules. Since DNA contains the assembly = instructions=20 for building proteins, the information-processing system in the cell = represents=20 a kind of communication channel (Yockey 1992:110). Further, DNA conveys=20 information via specifically arranged sequences of nucleotide bases. = Since each=20 of the four bases has a roughly equal chance of occurring at each site = along the=20 spine of the DNA molecule, biologists can calculate the probability, and = thus=20 the information-carrying capacity, of any particular sequence n = bases=20 long.

The ease with which information theory applies to molecular = biology=20 has created confusion about the type of information that DNA and = proteins=20 possess. Sequences of nucleotide bases in DNA, or amino acids in a = protein, are=20 highly improbable and thus have large information-carrying capacities. = But, like=20 meaningful sentences or lines of computer code, genes and proteins are = also=20 specified with respect to function. Just as the meaning of a = sentence=20 depends upon the specific arrangement of the letters in a sentence, so = too does=20 the function of a gene sequence depend upon the specific arrangement of = the=20 nucleotide bases in a gene. Thus, molecular biologists beginning with = Crick=20 equated information not only with complexity but also with = =93specificity,=94=20 where =93specificity=94 or =93specified=94 has meant =93necessary to = function=94 (Crick=20 1958:144, 153; Sarkar, 1996:191).³=20 Molecular biologists such as Monod and Crick understood biological=20 information--the information stored in DNA and proteins--as something = more than=20 mere complexity (or improbability). Their notion of information = associated both=20 biochemical contingency and combinatorial complexity with DNA sequences=20 (allowing DNA's carrying capacity to be calculated), but it also = affirmed that=20 sequences of nucleotides and amino acids in functioning macromolecules = possessed=20 a high degree of specificity relative to the maintenance of = cellular=20 function.

The ease with which information theory applies to = molecular=20 biology has also created confusion about the location of information in=20 organisms. Perhaps because the information carrying capacity of the gene = could=20 be so easily measured, it has been easy to treat DNA, RNA and proteins = as the=20 sole repositories of biological information. Neo-Darwinists in = particular have=20 assumed that the origination of biological form could be explained by = recourse=20 to processes of genetic variation and mutation alone (Levinton = 1988:485). Yet if=20 one understands organismal form as resulting from constraints on the = possible=20 arrangements of matter at many levels in the biological hierarchy--from = genes=20 and proteins to cell types and tissues to organs and body plans--then = clearly=20 biological organisms exhibit many levels of information-rich=20 structure.

Thus, we can pose a question, not only about the = origin of=20 genetic information, but also about the origin of the information = necessary to=20 generate form and structure at levels higher than that present in = individual=20 proteins. We must also ask about the origin of the =93specified = complexity,=94 as=20 opposed to mere complexity, that characterizes the new genes, proteins, = cell=20 types and body plans that arose in the Cambrian explosion. Dembski = (2002) has=20 used the term =93complex specified information=94 (CSI) as a synonym for = =93specified=20 complexity=94 to help distinguish functional biological information from = mere=20 Shannon information--that is, specified complexity from mere complexity. = This=20 review will use this term as well.

The Cambrian Information=20 Explosion

The Cambrian explosion represents a remarkable jump = in the=20 specified complexity or =93complex specified information=94 (CSI) of the = biological=20 world. For over three billions years, the biological realm included = little more=20 than bacteria and algae (Brocks et al. 1999). Then, beginning about = 570-565=20 million years ago (mya), the first complex multicellular organisms = appeared in=20 the rock strata, including sponges, cnidarians, and the peculiar = Ediacaran biota=20 (Grotzinger et al. 1995). Forty million years later, the Cambrian = explosion=20 occurred (Bowring et al. 1993). The emergence of the Ediacaran biota = (570 mya),=20 and then to a much greater extent the Cambrian explosion (530 mya), = represented=20 steep climbs up the biological complexity gradient.

One way to = estimate=20 the amount of new CSI that appeared with the Cambrian animals is to = count the=20 number of new cell types that emerged with them (Valentine 1995:91-93). = Studies=20 of modern animals suggest that the sponges that appeared in the late=20 Precambrian, for example, would have required five cell types, whereas = the more=20 complex animals that appeared in the Cambrian (e.g., arthropods) would = have=20 required fifty or more cell types. Functionally more complex animals = require=20 more cell types to perform their more diverse functions. New cell types = require=20 many new and specialized proteins. New proteins, in turn, require new = genetic=20 information. Thus an increase in the number of cell types implies (at a = minimum)=20 a considerable increase in the amount of specified genetic information.=20 Molecular biologists have recently estimated that a minimally complex=20 single-celled organism would require between 318 and 562 kilobase pairs = of DNA=20 to produce the proteins necessary to maintain life (Koonin 2000). More = complex=20 single cells might require upward of a million base pairs. Yet to build = the=20 proteins necessary to sustain a complex arthropod such as a trilobite = would=20 require orders of magnitude more coding instructions. The genome size of = a=20 modern arthropod, the fruitfly Drosophila melanogaster, is = approximately=20 180 million base pairs (Gerhart & Kirschner 1997:121, Adams et al. = 2000).=20 Transitions from a single cell to colonies of cells to complex animals = represent=20 significant (and, in principle, measurable) increases in = CSI.

Building a=20 new animal from a single-celled organism requires a vast amount of new = genetic=20 information. It also requires a way of arranging gene = products--proteins--into=20 higher levels of organization. New proteins are required to service new = cell=20 types. But new proteins must be organized into new systems within the = cell; new=20 cell types must be organized into new tissues, organs, and body parts. = These, in=20 turn, must be organized to form body plans. New animals, therefore, = embody=20 hierarchically organized systems of lower-level parts within a = functional whole.=20 Such hierarchical organization itself represents a type of information, = since=20 body plans comprise both highly improbable and functionally specified=20 arrangements of lower-level parts. The specified complexity of new body = plans=20 requires explanation in any account of the Cambrian = explosion.

Can=20 neo-Darwinism explain the discontinuous increase in CSI that appears in = the=20 Cambrian explosion--either in the form of new genetic information or in = the form=20 of hierarchically organized systems of parts? We will now examine the = two parts=20 of this question.

Novel Genes and Proteins

Many = scientists=20 and mathematicians have questioned the ability of mutation and selection = to=20 generate information in the form of novel genes and proteins. Such = skepticism=20 often derives from consideration of the extreme improbability (and = specificity)=20 of functional genes and proteins.

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

Since the 1960s, some biologists have thought = functional=20 proteins to be rare among the set of possible amino acid sequences. Some = have=20 used an analogy with human language to illustrate why this should be the = case.=20 Denton (1986, 309-311), for example, has shown that meaningful words and = sentences are extremely rare among the set of possible combinations of = English=20 letters, especially as sequence length grows. (The ratio of meaningful = 12-letter=20 words to 12-letter sequences is 1/10¹⁴, the ratio of = 100-letter=20 sentences to possible 100-letter strings is 1/10100.) Further, Denton = shows that=20 most meaningful sentences are highly isolated from one another in = the=20 space of possible combinations, so that random substitutions of letters = will,=20 after a very few changes, inevitably degrade meaning. Apart from a few = closely=20 clustered sentences accessible by random substitution, the overwhelming = majority=20 of meaningful sentences lie, probabilistically speaking, beyond the = reach of=20 random search.

Denton (1986:301-324) and others have argued that = similar=20 constraints apply to genes and proteins. They have questioned whether an = undirected search via mutation and selection would have a reasonable = chance of=20 locating new islands of function--representing fundamentally new genes = or=20 proteins--within the time available (Eden 1967, Shutzenberger 1967, = Lovtrup=20 1979). Some have also argued that alterations in sequencing would likely = result=20 in loss of protein function before fundamentally new function could = arise (Eden=20 1967, Denton 1986). Nevertheless, neither the extent to which genes and = proteins=20 are sensitive to functional loss as a result of sequence change, nor the = extent=20 to which functional proteins are isolated within sequence space, has = been fully=20 known.

Recently, experiments in molecular biology have shed light = on=20 these questions. A variety of mutagenesis techniques have shown that = proteins=20 (and thus the genes that produce them) are indeed highly specified = relative to=20 biological function (Bowie & Sauer 1989, Reidhaar-Olson & Sauer = 1990,=20 Taylor et al. 2001). Mutagenesis research tests the sensitivity of = proteins=20 (and, by implication, DNA) to functional loss as a result of alterations = in=20 sequencing. Studies of proteins have long shown that amino acid residues = at many=20 active positions cannot vary without functional loss (Perutz & = Lehmann=20 1968). More recent protein studies (often using mutagenesis experiments) = have=20 shown that functional requirements place significant constraints on = sequencing=20 even at non-active site positions (Bowie & Sauer 1989, = Reidhaar-Olson &=20 Sauer 1990, Chothia et al. 1998, Axe 2000, Taylor et al. 2001). In = particular,=20 Axe (2000) has shown that multiple as opposed to single position amino = acid=20 substitutions inevitably result in loss of protein function, even when = these=20 changes occur at sites that allow variation when altered in isolation.=20 Cumulatively, these constraints imply that proteins are highly sensitive = to=20 functional loss as a result of alterations in sequencing, and that = functional=20 proteins represent highly isolated and improbable arrangements of amino = acids=20 -arrangements that are far more improbable, in fact, than would be = likely to=20 arise by chance alone in the time available (Reidhaar-Olson & Sauer = 1990;=20 Behe 1992; Kauffman 1995:44; Dembski 1998:175-223; Axe 2000, 2004). (See = below=20 the discussion of the neutral theory of evolution for a precise = quantitative=20 assessment.)

Of course, neo-Darwinists do not envision a = completely=20 random search through the set of all possible nucleotide = sequences--so-called=20 =93sequence space.=94 They envision natural selection acting to preserve = small=20 advantageous variations in genetic sequences and their corresponding = protein=20 products. Dawkins (1996), for example, likens an organism to a high = mountain=20 peak. He compares climbing the sheer precipice up the front side of the = mountain=20 to building a new organism by chance. He acknowledges that his approach = up=20 =93Mount Improbable=94 will not succeed. Nevertheless, he suggests that = there is a=20 gradual slope up the backside of the mountain that could be climbed in = small=20 incremental steps. In his analogy, the backside climb up =93Mount = Improbable=94=20 corresponds to the process of natural selection acting on random changes = in the=20 genetic text. What chance alone cannot accomplish blindly or in one = leap,=20 selection (acting on mutations) can accomplish through the cumulative = effect of=20 many slight successive steps.

Yet the extreme specificity and = complexity=20 of proteins presents a difficulty, not only for the chance origin of = specified=20 biological information (i.e., for random mutations acting alone), but = also for=20 selection and mutation acting in concert. Indeed, mutagenesis = experiments cast=20 doubt on each of the two scenarios by which neo-Darwinists envisioned = new=20 information arising from the mutation/selection mechanism (for review, = see=20 Lonnig 2001). For neo-Darwinism, new functional genes either arise from=20 non-coding sections in the genome or from preexisting genes. Both = scenarios are=20 problematic.

In the first scenario, neo-Darwinists envision new = genetic=20 information arising from those sections of the genetic text that can = presumably=20 vary freely without consequence to the organism. According to this = scenario,=20 non-coding sections of the genome, or duplicated sections of coding = regions, can=20 experience a protracted period of =93neutral evolution=94 (Kimura 1983) = during which=20 alterations in nucleotide sequences have no discernible effect on the = function=20 of the organism. Eventually, however, a new gene sequence will arise = that can=20 code for a novel protein. At that point, natural selection can favor the = new=20 gene and its functional protein product, thus securing the preservation = and=20 heritability of both.

This scenario has the advantage of allowing = the=20 genome to vary through many generations, as mutations =93search=94 the = space of=20 possible base sequences. The scenario has an overriding problem, = however: the=20 size of the combinatorial space (i.e., the number of possible amino acid = sequences) and the extreme rarity and isolation of the functional = sequences=20 within that space of possibilities. Since natural selection can do = nothing to=20 help generate new functional sequences, but rather can only = preserve such=20 sequences once they have arisen, chance alone--random variation--must do = the=20 work of information generation--that is, of finding the exceedingly rare = functional sequences within the set of combinatorial possibilities. Yet = the=20 probability of randomly assembling (or =93finding,=94 in the previous = sense) a=20 functional sequence is extremely small.

Cassette mutagenesis = experiments=20 performed during the early 1990s suggest that the probability of = attaining (at=20 random) the correct sequencing for a short protein 100 amino acids long = is about=20 1 in 10⁶⁵ (Reidhaar-Olson & Sauer 1990, Behe 1992:65-69). = This=20 result agreed closely with earlier calculations that Yockey (1978) had = performed=20 based upon the known sequence variability of cytochrome c in different = species=20 and other theoretical considerations. More recent mutagenesis research = has=20 provided additional support for the conclusion that functional proteins = are=20 exceedingly rare among possible amino acid sequences (Axe 2000, 2004). = Axe=20 (2004) has performed site directed mutagenesis experiments on a = 150-residue=20 protein-folding domain within a B-lactamase enzyme. His experimental = method=20 improves upon earlier mutagenesis techniques and corrects for several = sources of=20 possible estimation error inherent in them. On the basis of these = experiments,=20 Axe has estimated the ratio of (a) proteins of typical size (150 = residues) that=20 perform a specified function via any folded structure to (b) the whole = set of=20 possible amino acids sequences of that size. Based on his experiments, = Axe has=20 estimated his ratio to be 1 to 10⁷⁷. Thus, the probability of = finding=20 a functional protein among the possible amino acid sequences = corresponding to a=20 150-residue protein is similarly 1 in 10⁷⁷.

Other=20 considerations imply additional improbabilities. First, new Cambrian = animals=20 would require proteins much longer than 100 residues to perform many = necessary=20 specialized functions. Ohno (1996) has noted that Cambrian animals would = have=20 required complex proteins such as lysyl oxidase in order to support = their stout=20 body structures. Lysyl oxidase molecules in extant organisms comprise = over 400=20 amino acids. These molecules are both highly complex (non-repetitive) = and=20 functionally specified. Reasonable extrapolation from mutagenesis = experiments=20 done on shorter protein molecules suggests that the probability of = producing=20 functionally sequenced proteins of this length at random is so small as = to make=20 appeals to chance absurd, even granting the duration of the entire = universe.=20 (See Dembski 1998:175-223 for a rigorous calculation of this = =93Universal=20 Probability Bound=94; See also Axe 2004.) Yet, second, fossil data = (Bowring et al.=20 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,=20 7 x 10⁷ years) is far smaller than that of the entire = universe (1.3-2=20 x 10¹⁰ years). Third, DNA mutation rates are far too low to = generate=20 the novel genes and proteins necessary to building the Cambrian animals, = given=20 the most probable duration of the explosion as determined by fossil = studies=20 (Conway Morris 1998b). As Ohno (1996:8475) notes, even a mutation rate = of=20 10-⁹ per base pair per year results in only a 1% change in = the=20 sequence of a given section of DNA in 10 million years. Thus, he argues = that=20 mutational divergence of preexisting genes cannot explain the origin of = the=20 Cambrian forms in that time.⁴

The=20 selection/mutation mechanism faces another probabilistic obstacle. The = animals=20 that arise in the Cambrian exhibit structures that would have required = many new=20 types of cells, each of which would have required many novel = proteins to=20 perform their specialized functions. Further, new cell types require=20 Asystems of proteins that must, as a condition of functioning, = act in=20 close coordination with one another. The unit of selection in such = systems=20 ascends to the system as a whole. Natural selection selects for = functional=20 advantage. But new cell types require whole systems of proteins to = perform their=20 distinctive functions. In such cases, natural selection cannot = contribute to the=20 process of information generation until after the information = necessary=20 to build the requisite system of proteins has arisen. Thus random = variations must, again, do the work of information generation--and now = not=20 simply for one protein, but for many proteins arising at nearly the same = time.=20 Yet the odds of this occurring by chance alone are, of course, far = smaller than=20 the odds of the chance origin of a single gene or protein--so small in = fact as=20 to render the chance origin of the genetic information necessary to = build a new=20 cell type (a necessary but not sufficient condition of building a new = body plan)=20 problematic given even the most optimistic estimates for the duration of = the=20 Cambrian explosion.

Dawkins (1986:139) has noted that scientific = theories=20 can rely on only so much =93luck=94 before they cease to be credible. = The neutral=20 theory of evolution, which, by its own logic, prevents natural selection = from=20 playing a role in generating genetic information until after the fact, = relies on=20 entirely too much luck. The sensitivity of proteins to functional loss, = the need=20 for long proteins to build new cell types and animals, the need for = whole new=20 systems of proteins to service new cell types, the probable = brevity of=20 the Cambrian explosion relative to mutation rates--all suggest the = immense=20 improbability (and implausibility) of any scenario for the origination = of=20 Cambrian genetic information that relies upon random variation alone = unassisted=20 by natural selection.

Yet the neutral theory requires novel genes = and=20 proteins to arise--essentially--by random mutation alone. Adaptive = advantage=20 accrues after the generation of new functional genes and = proteins. Thus,=20 natural selection cannot play a role until new = information-bearing=20 molecules have independently arisen. Thus neutral theorists envisioned = the need=20 to scale the steep face of a Dawkins-style precipice of which there is = no=20 gradually sloping backside--a situation that, by Dawkins' own logic, is=20 probabilistically untenable.

In the second scenario, = neo-Darwinists=20 envisioned novel genes and proteins arising by numerous successive = mutations in=20 the preexisting genetic text that codes for proteins. To adapt Dawkins's = metaphor, this scenario envisions gradually climbing down one functional = peak=20 and then ascending another. Yet mutagenesis experiments again suggest a=20 difficulty. Recent experiments show that, even when exploring a region = of=20 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=20 turn one protein into another with a completely novel structure and = function=20 requires specified changes at many sites. Indeed, the number of changes=20 necessary to produce a new protein greatly exceeds the number of changes = that=20 will typically produce functional losses. Given this, the probability of = escaping total functional loss during a random search for the changes = needed to=20 produce a new function is extremely small--and this probability = diminishes=20 exponentially with each additional requisite change (Axe 2000). Thus, = Axe's=20 results imply that, in all probability, random searches for novel = proteins=20 (through sequence space) will result in functional loss long before any = novel=20 functional protein will emerge.

Blanco et al. have come to a = similar=20 conclusion. Using directed mutagenesis, they have determined that = residues in=20 both the hydrophobic core and on the surface of the protein play = essential roles=20 in determining protein structure. By sampling intermediate sequences = between two=20 naturally occurring sequences that adopt different folds, they found = that the=20 intermediate sequences =93lack a well defined three-dimensional = structure.=94 Thus,=20 they conclude that it is unlikely that a new protein fold via a series = of folded=20 intermediates sequences (Blanco et al. 1999:741).

Thus, although = this=20 second neo-Darwinian scenario has the advantage of starting with = functional=20 genes and proteins, it also has a lethal disadvantage: any process of = random=20 mutation or rearrangement in the genome would in all probability = generate=20 nonfunctional intermediate sequences before fundamentally new functional = genes=20 or proteins would arise. Clearly, nonfunctional intermediate sequences = confer no=20 survival advantage on their host organisms. Natural selection favors = only=20 functional advantage. It cannot select or favor nucleotide sequences or=20 polypeptide chains that do not yet perform biological functions, and = still less=20 will it favor sequences that efface or destroy preexisting=20 function.

Evolving genes and proteins will range through a series = of=20 nonfunctional intermediate sequences that natural selection will not = favor or=20 preserve but will, in all probability, eliminate (Blanco et al. 1999, = Axe 2000).=20 When this happens, selection-driven evolution will cease. At this point, = neutral=20 evolution of the genome (unhinged from selective pressure) may ensue, = but, as we=20 have seen, such a process must overcome immense probabilistic hurdles, = even=20 granting cosmic time.

Thus, whether one envisions the = evolutionary=20 process beginning with a noncoding region of the genome or a preexisting = functional gene, the functional specificity and complexity of proteins = impose=20 very stringent limitations on the efficacy of mutation and selection. In = the=20 first case, function must arise first, before natural selection can act = to favor=20 a novel variation. In the second case, function must be continuously = maintained=20 in order to prevent deleterious (or lethal) consequences to the organism = and to=20 allow further evolution. Yet the complexity and functional specificity = of=20 proteins implies that both these conditions will be extremely difficult = to meet.=20 Therefore, the neo-Darwinian mechanism appears to be inadequate to = generate the=20 new information present in the novel genes and proteins that arise with = the=20 Cambrian animals.

Novel Body Plans

The problems = with the=20 neo-Darwinian mechanism run deeper still. In order to explain the origin = of the=20 Cambrian animals, one must account not only for new proteins and cell = types, but=20 also for the origin of new body plans. Within the past decade, = developmental=20 biology has dramatically advanced our understanding of how body plans = are built=20 during ontogeny. In the process, it has also uncovered a profound = difficulty for=20 neo-Darwinism.

Significant morphological change in organisms = requires=20 attention to timing. Mutations in genes that are expressed late in the=20 development of an organism will not affect the body plan. Mutations = expressed=20 early in development, however, could conceivably produce significant=20 morphological change (Arthur 1997:21). Thus, events expressed early in = the=20 development of organisms have the only realistic chance of producing = large-scale=20 macroevolutionary change (Thomson 1992). As John and Miklos (1988:309) = explain,=20 macroevolutionary change requires alterations in the very early stages = of=20 ontogenesis.

Yet recent studies in developmental biology make = clear that=20 mutations expressed early in development typically have deleterious = effects=20 (Arthur 1997:21). For example, when early-acting body plan molecules, or = morphogens such as bicoid (which helps to set up the = anterior-posterior=20 head-to-tail axis in Drosophila), are perturbed, development = shuts down=20 (Nusslein-Volhard & Wieschaus 1980, Lawrence & Struhl 1996, = Muller &=20 Newman 2003).⁵=20 The resulting embryos die. Moreover, there is a good reason for this. If = an=20 engineer modifies the length of the piston rods in an internal = combustion engine=20 without modifying the crankshaft accordingly, the engine won't start. = Similarly,=20 processes of development are tightly integrated spatially and temporally = such=20 that changes early in development will require a host of other = coordinated=20 changes in separate but functionally interrelated developmental = processes=20 downstream. For this reason, mutations will be much more likely to be = deadly if=20 they disrupt a functionally deeply-embedded structure such as a spinal = column=20 than if they affect more isolated anatomical features such as fingers = (Kauffman=20 1995:200).

This problem has led to what McDonald (1983) has = called =93a=20 great Darwinian paradox=94 (p. 93). McDonald notes that genes that are = observed to=20 vary within natural populations do not lead to major adaptive changes, = while=20 genes that could cause major changes--the very stuff of=20 macroevolution--apparently do not vary. In other words, mutations of the = kind=20 that macroevolution doesn't need (namely, viable genetic mutations in = DNA=20 expressed late in development) do occur, but those that it does need = (namely,=20 beneficial body plan mutations expressed early in development) = apparently don't=20 occur.⁶=20 According to Darwin (1859:108) natural selection cannot act until = favorable=20 variations arise in a population. Yet there is no evidence from = developmental=20 genetics that the kind of variations required by neo-Darwinism--namely,=20 favorable body plan mutations--ever occur.

Developmental biology = has=20 raised another formidable problem for the mutation/selection mechanism.=20 Embryological evidence has long shown that DNA does not wholly determine = morphological form (Goodwin 1985, Nijhout 1990, Sapp 1987, Muller & = Newman=20 2003), suggesting that mutations in DNA alone cannot account for the=20 morphological changes required to build a new body plan.

DNA = helps direct=20 protein synthesis.⁷=20 It also helps to regulate the timing and expression of the synthesis of = various=20 proteins within cells. Yet, DNA alone does not determine how individual = proteins=20 assemble themselves into larger systems of proteins; still less does it = solely=20 determine how cell types, tissue types, and organs arrange themselves = into body=20 plans (Harold 1995:2774, Moss 2004). Instead, other factors--such as the = three-dimensional structure and organization of the cell membrane and=20 cytoskeleton and the spatial architecture of the fertilized egg--play = important=20 roles in determining body plan formation during = embryogenesis.

For=20 example, the structure and location of the cytoskeleton influence the = patterning=20 of embryos. Arrays of microtubules help to distribute the essential = proteins=20 used during development to their correct locations in the cell. Of = course,=20 microtubules themselves are made of many protein subunits. Nevertheless, = like=20 bricks that can be used to assemble many different structures, the = tubulin=20 subunits in the cell's microtubules are identical to one another. Thus, = neither=20 the tubulin subunits nor the genes that produce them account for the = different=20 shape of microtubule arrays that distinguish different kinds of embryos = and=20 developmental pathways. Instead, the structure of the microtubule array = itself=20 is determined by the location and arrangement of its subunits, not the=20 properties of the subunits themselves. For this reason, it is not = possible to=20 predict the structure of the cytoskeleton of the cell from the = characteristics=20 of the protein constituents that form that structure (Harold=20 2001:125).

Two analogies may help further clarify the point. At a = building site, builders will make use of many materials: lumber, wires, = nails,=20 drywall, piping, and windows. Yet building materials do not determine = the floor=20 plan of the house, or the arrangement of houses in a neighborhood. = Similarly,=20 electronic circuits are composed of many components, such as resistors,=20 capacitors, and transistors. But such lower-level components do not = determine=20 their own arrangement in an integrated circuit. Biological symptoms also = depend=20 on hierarchical arrangements of parts. Genes and proteins are made from = simple=20 building blocks--nucleotide bases and amino acids--arranged in specific = ways.=20 Cell types are made of, among other things, systems of specialized = proteins.=20 Organs are made of specialized arrangements of cell types and tissues. = And body=20 plans comprise specific arrangements of specialized organs. Yet, = clearly, the=20 properties of individual proteins (or, indeed, the lower-level parts in = the=20 hierarchy generally) do not fully determine the organization of the = higher-level=20 structures and organizational patterns (Harold 2001:125). It follows = that the=20 genetic information that codes for proteins does not determine these=20 higher-level structures either.

These considerations pose another = challenge to the sufficiency of the neo-Darwinian mechanism. = Neo-Darwinism seeks=20 to explain the origin of new information, form, and structure as a = result of=20 selection acting on randomly arising variation at a very low level = within the=20 biological hierarchy, namely, within the genetic text. Yet major = morphological=20 innovations depend on a specificity of arrangement at a much higher = level of the=20 organizational hierarchy, a level that DNA alone does not determine. Yet = if DNA=20 is not wholly responsible for body plan morphogenesis, then DNA = sequences can=20 mutate indefinitely, without regard to realistic probabilistic limits, = and still=20 not produce a new body plan. Thus, the mechanism of natural selection = acting on=20 random mutations in DNA cannot in principle generate novel body = plans,=20 including those that first arose in the Cambrian explosion.

Of = course, it=20 could be argued that, while many single proteins do not by themselves = determine=20 cellular structures and/or body plans, proteins acting in concert with = other=20 proteins or suites of proteins could determine such higher-level form. = For=20 example, it might be pointed out that the tubulin subunits (cited above) = are=20 assembled by other helper proteins--gene products--called Microtubule = Associated=20 Proteins (MAPS). This might seem to suggest that genes and gene products = alone=20 do suffice to determine the development of the three-dimensional = structure of=20 the cytoskeleton.

Yet MAPS, and indeed many other necessary = proteins, are=20 only part of the story. The location of specified target sites on the = interior=20 of the cell membrane also helps to determine the shape of the = cytoskeleton.=20 Similarly, so does the position and structure of the centrosome which = nucleates=20 the microtubules that form the cytoskeleton. While both the membrane = targets and=20 the centrosomes are made of proteins, the location and form of these = structures=20 is not wholly determined by the proteins that form them. Indeed, = centrosome=20 structure and membrane patterns as a whole convey = three-dimensional=20 structural information that helps determine the structure of the = cytoskeleton=20 and the location of its subunits (McNiven & Porter 1992:313-329). = Moreover,=20 the centrioles that compose the centrosomes replicate independently of = DNA=20 replication (Lange et al. 2000:235-249, Marshall & Rosenbaum = 2000:187-205).=20 The daughter centriole receives its form from the overall structure of = the=20 mother centriole, not from the individual gene products that constitute = it=20 (Lange et al. 2000). In ciliates, microsurgery on cell membranes can = produce=20 heritable changes in membrane patterns, even though the DNA of the = ciliates has=20 not been altered (Sonneborn 1970:1-13, Frankel 1980:607-623; Nanney=20 1983:163-170). This suggests that membrane patterns (as opposed to = membrane=20 constituents) are impressed directly on daughter cells. In both cases, = form is=20 transmitted from parent three-dimensional structures to daughter=20 three-dimensional structures directly and is not wholly contained in = constituent=20 proteins or genetic information (Moss 2004).

Thus, in each new=20 generation, the form and structure of the cell arises as the result of=20 both gene products and preexisting three-dimensional structure = and=20 organization. Cellular structures are built from proteins, but proteins = find=20 their way to correct locations in part because of preexisting = three-dimensional=20 patterns and organization inherent in cellular structures. Preexisting=20 three-dimensional form present in the preceding generation (whether = inherent in=20 the cell membrane, the centrosomes, the cytoskeleton or other features = of the=20 fertilized egg) contributes to the production of form in the next = generation.=20 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=20 conditions, for the development of three-dimensional structure within = cells,=20 organs and body plans (Harold 1995:2767). But if this is so, then = natural=20 selection acting on genetic variation alone cannot produce the new forms = that=20 arise in history of life.

Self-Organizational = Models

Of=20 course, neo-Darwinism is not the only evolutionary theory for explaining = the=20 origin of novel biological form. Kauffman (1995) doubts the efficacy of = the=20 mutation/selection mechanism. Nevertheless, he has advanced a=20 self-organizational theory to account for the emergence of new form, and = presumably the information necessary to generate it. Whereas = neo-Darwinism=20 attempts to explain new form as the consequence of selection acting on = random=20 mutation, Kauffman suggests that selection acts, not mainly on random=20 variations, but on emergent patterns of order that self-organize via the = laws of=20 nature.

Kauffman (1995:47-92) illustrates how this might work = with=20 various model systems in a computer environment. In one, he conceives a = system=20 of buttons connected by strings. Buttons represent novel genes or gene = products;=20 strings represent the law-like forces of interaction that obtain between = gene=20 products-i.e., proteins. Kauffman suggests that when the complexity of = the=20 system (as represented by the number of buttons and strings) reaches a = critical=20 threshold, new modes of organization can arise in the system =93for = free=94--that=20 is, naturally and spontaneously--after the manner of a phase transition = in=20 chemistry.

Another model that Kauffman develops is a system of=20 interconnected lights. Each light can flash in a variety of states--on, = off,=20 twinkling, etc. Since there is more than one possible state for each = light, and=20 many lights, there are a vast number of possible states that the system = can=20 adopt. Further, in his system, rules determine how past states will = influence=20 future states. Kauffman asserts that, as a result of these rules, the = system=20 will, if properly tuned, eventually produce a kind of order in which a = few basic=20 patterns of light activity recur with greater-than-random frequency. = Since these=20 actual patterns of light activity represent a small portion of the total = number=20 of possible states in which the system can reside, Kauffman seems to = imply that=20 self-organizational laws might similarly result in highly improbable = biological=20 outcomes--perhaps even sequences (of bases or amino acids) within a much = larger=20 sequence space of possibilities.

Do these simulations of=20 self-organizational processes accurately model the origin of novel = genetic=20 information? It is hard to think so.

First, in both examples, = Kauffman=20 presupposes but does not explain significant sources of preexisting = information.=20 In his buttons-and-strings system, the buttons represent proteins, = themselves=20 packets of CSI, and the result of preexisting genetic information. Where = does=20 this information come from? Kauffman (1995) doesn't say, but the origin = of such=20 information is an essential part of what needs to be explained in the = history of=20 life. Similarly, in his light system, the order that allegedly arises = for =93for=20 free=94 actually arises only if the programmer of the model system = =93tunes=94 it in=20 such a way as to keep it from either (a) generating an excessively rigid = order=20 or (b) developing into chaos (pp. 86-88). Yet this necessary tuning = involves an=20 intelligent programmer selecting certain parameters and excluding = others--that=20 is, inputting information.

Second, Kauffman's model systems are = not=20 constrained by functional considerations and thus are not analogous to=20 biological systems. A system of interconnected lights governed by = pre-programmed=20 rules may well settle into a small number of patterns within a much = larger space=20 of possibilities. But because these patterns have no function, and need = not meet=20 any functional requirements, they have no specificity analogous to that = present=20 in actual organisms. Instead, examination of Kauffman's (1995) model = systems=20 shows that they do not produce sequences or systems characterized by=20 specified complexity, but instead by large amounts of symmetrical = order=20 or internal redundancy interspersed with aperiodicity or (mere) = complexity (pp.=20 53, 89, 102). Getting a law-governed system to generate repetitive = patterns of=20 flashing lights, even with a certain amount of variation, is clearly=20 interesting, but not biologically relevant. On the other hand, a system = of=20 lights flashing the title of a Broadway play would model a biologically = relevant=20 self-organizational process, at least if such a meaningful or = functionally=20 specified sequence arose without intelligent agents previously = programming the=20 system with equivalent amounts of CSI. In any case, Kauffman's systems = do not=20 produce specified complexity, and thus do not offer promising = models for=20 explaining the new genes and proteins that arose in the = Cambrian.

Even=20 so, Kauffman suggests that his self-organizational models can = specifically=20 elucidate aspects of the Cambrian explosion. According to Kauffman=20 (1995:199-201), new Cambrian animals emerged as the result of =93long = jump=94=20 mutations that established new body plans in a discrete rather than = gradual=20 fashion. He also recognizes that mutations affecting early development = are=20 almost inevitably harmful. Thus, he concludes that body plans, once = established,=20 will not change, and that any subsequent evolution must occur within an=20 established body plan (Kauffman 1995:201). And indeed, the fossil record = does=20 show a curious (from a neo-Darwinian point of view) top-down pattern of=20 appearance, in which higher taxa (and the body plans they represent) = appear=20 first, only later to be followed by the multiplication of lower taxa=20 representing variations within those original body designs (Erwin et al. = 1987,=20 Lewin 1988, Valentine & Jablonski 2003:518). Further, as Kauffman = expects,=20 body plans appear suddenly and persist without significant modification = over=20 time.

But here, again, Kauffman begs the most important question, = which=20 is: what produces the new Cambrian body plans in the first place? = Granted, he=20 invokes =93long jump mutations=94 to explain this, but he identifies no = specific=20 self-organizational process that can produce such mutations. Moreover, = he=20 concedes a principle that undermines the plausibility of his own = proposal.=20 Kauffman acknowledges that mutations that occur early in development are = almost=20 inevitably deleterious. Yet developmental biologists know that these are = the=20 only kind of mutations that have a realistic chance of producing = large-scale=20 evolutionary change--i.e., the big jumps that Kauffman invokes. Though = Kauffman=20 repudiates the neo-Darwinian reliance upon random mutations in favor of=20 self-organizing order, in the end, he must invoke the most implausible = kind of=20 random mutation in order to provide a self-organizational account of the = new=20 Cambrian body plans. Clearly, his model is not = sufficient.

Punctuated=20 Equilibrium

Of course, still other causal explanations have = been=20 proposed. During the 1970s, the paleontologists Eldredge and Gould = (1972)=20 proposed the theory of evolution by punctuated equilibrium in order to = account=20 for a pervasive pattern of =93sudden appearance=94 and =93stasis=94 in = the fossil=20 record. Though advocates of punctuated equilibrium were mainly seeking = to=20 describe the fossil record more accurately than earlier gradualist = neo-Darwinian=20 models had done, they did also propose a mechanism--known as species=20 selection--by which the large morphological jumps evident in fossil = record might=20 have been produced. According to punctuationalists, natural selection = functions=20 more as a mechanism for selecting the fittest species rather than the = most-fit=20 individual among a species. Accordingly, on this model, morphological = change=20 should occur in larger, more discrete intervals than it would given a=20 traditional neo-Darwinian understanding.

Despite its virtues as a = descriptive model of the history of life, punctuated equilibrium has = been widely=20 criticized for failing to provide a mechanism sufficient to produce the = novel=20 form characteristic of higher taxonomic groups. For one thing, critics = have=20 noted that the proposed mechanism of punctuated evolutionary change = simply=20 lacked the raw material upon which to work. As Valentine and Erwin = (1987) note,=20 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=20 pool of species upon which to act. Thus, they conclude that the = mechanism of=20 species selection probably does not resolve the problem of the origin of = the=20 higher taxonomic groups (p. 96).⁸=20 Further, punctuated equilibrium has not addressed the more specific and=20 fundamental problem of explaining the origin of the new biological = information=20 (whether genetic or epigenetic) necessary to produce novel biological = form.=20 Advocates of punctuated equilibrium might assume that the new species = (upon=20 which natural selection acts) arise by known microevolutionary processes = of=20 speciation (such as founder effect, genetic drift or bottleneck effect) = that do=20 not necessarily depend upon mutations to produce adaptive changes. But, = in that=20 case, the theory lacks an account of how the specifically higher = taxa=20 arise. Species selection will only produce more fit species. On the = other hand,=20 if punctuationalists assume that processes of genetic mutation can = produce more=20 fundamental morphological changes and variations, then their model = becomes=20 subject to the same problems as neo-Darwinism (see above). This dilemma = is=20 evident in Gould (2002:710) insofar as his attempts to explain adaptive=20 complexity inevitably employ classical neo-Darwinian modes of = explanation^.9

Structuralism

= Another=20 attempt to explain the origin of form has been proposed by the = structuralists=20 such as Gerry Webster and Brian Goodwin (1984, 1996). These biologists, = drawing=20 on the earlier work of D'Arcy Thompson (1942), view biological form as = the=20 result of structural constraints imposed upon matter by morphogenetic = rules or=20 laws. For reasons similar to those discussed above, the structuralists = have=20 insisted that these generative or morphogenetic rules do not reside in = the lower=20 level building materials of organisms, whether in genes or proteins. = Webster and=20 Goodwin (1984:510-511) further envisioned morphogenetic rules or laws = operating=20 ahistorically, similar to the way in which gravitational or = electromagnetic laws=20 operate. For this reason, structuralists see phylogeny as of secondary=20 importance in understanding the origin of the higher taxa, though they = think=20 that transformations of form can occur. For structuralists, constraints = on the=20 arrangement of matter arise not mainly as the result of historical=20 contingencies--such as environmental changes or genetic mutations--but = instead=20 because of the continuous ahistorical operation of fundamental laws of=20 form--laws that organize or inform matter.

While this approach = avoids=20 many of the difficulties currently afflicting neo-Darwinism (in = particular those=20 associated with its =93genocentricity=94), critics (such as Maynard = Smith 1986) of=20 structuralism have argued that the structuralist explanation of form = lacks=20 specificity. They note that structuralists have been unable to say just = where=20 laws of form reside--whether in the universe, or in every possible = world, or in=20 organisms as a whole, or in just some part of organisms. Further, = according to=20 structuralists, morphogenetic laws are mathematical in character. Yet,=20 structuralists have yet to specify the mathematical formulae that = determine=20 biological forms.

Others (Yockey 1992; Polanyi 1967, 1968; Meyer = 2003)=20 have questioned whether physical laws could in principle generate the = kind of=20 complexity that characterizes biological systems. Structuralists = envision the=20 existence of biological laws that produce form in much the same way that = physical laws produce form. Yet the forms that physicists regard as=20 manifestations of underlying laws are characterized by large amounts of=20 symmetric or redundant order, by relatively simple patterns such as = vortices or=20 gravitational fields or magnetic lines of force. Indeed, physical laws = are=20 typically expressed as differential equations (or algorithms) that = almost by=20 definition describe recurring phenomena--patterns of compressible = =93order=94 not=20 =93complexity=94 as defined by algorithmic information theory (Yockey = 1992:77-83).=20 Biological forms, by contrast, manifest greater complexity and derive in = ontogeny from highly complex initial conditions--i.e., non-redundant = sequences=20 of nucleotide bases in the genome and other forms of information = expressed in=20 the complex and irregular three-dimensional topography of the organism = or the=20 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=20 (algorithmic) complexity. Further, physical laws lack the information = content to=20 specify biology systems. As Polyanyi (1967, 1968) and Yockey (1992:290) = have=20 shown, the laws of physics and chemistry allow, but do not determine,=20 distinctively biological modes of organization. In other words, living = systems=20 are consistent with, but not deducible, from physical-chemical laws=20 (1992:290).

Of course, biological systems do manifest some = reoccurring=20 patterns, processes and behaviors. The same type of organism develops = repeatedly=20 from similar ontogenetic processes in the same species. Similar = processes of=20 cell division reoccur in many organisms. Thus, one might describe = certain=20 biological processes as law-governed. Even so, the existence of such = biological=20 regularities does not solve the problem of the origin of form and = information,=20 since the recurring processes described by such biological laws (if = there be=20 such laws) only occur as the result of preexisting stores of (genetic = and/or=20 epigenetic) information and these information-rich initial conditions = impose the=20 constraints that produce the recurring behavior in biological systems. = (For=20 example, processes of cell division recur with great frequency in = organisms, but=20 depend upon information-rich DNA and proteins molecules.) In other = words,=20 distinctively biological regularities depend upon preexisting biological = information. Thus, appeals to higher-level biological laws presuppose, = but do=20 not explain, the origination of the information necessary to=20 morphogenesis.

Thus, structuralism faces a difficult in principle = dilemma. On the one hand, physical laws produce very simple redundant = patterns=20 that lack the complexity characteristic of biological systems. On the = other=20 hand, distinctively biological laws--if there are such laws--depend upon = preexisting information-rich structures. In either case, laws are not = good=20 candidates for explaining the origination of biological form or the = information=20 necessary to produce it.

Cladism: An Artifact of=20 Classification?

Some cladists have advanced another approach = to the=20 problem of the origin of form, specifically as it arises in the = Cambrian. They=20 have argued that the problem of the origin of the phyla is an artifact = of the=20 classification system, and therefore, does not require explanation. Budd = and=20 Jensen (2000), for example, argue that the problem of the Cambrian = explosion=20 resolves itself if one keeps in mind the cladistic distinction between = =93stem=94=20 and =93crown=94 groups. Since crown groups arise whenever new characters = are added=20 to simpler more ancestral stem groups during the evolutionary process, = new phyla=20 will inevitably arise once a new stem group has arisen. Thus, for Budd = and=20 Jensen what requires explanation is not the crown groups corresponding = to the=20 new Cambrian phyla, but the earlier more primitive stem groups that = presumably=20 arose deep in the Proterozoic. Yet since these earlier stem groups are = by=20 definition less derived, explaining them will be considerably easier = than=20 explaining the origin of the Cambrian animals de novo. In any = case, for=20 Budd and Jensen the explosion of new phyla in the Cambrian does not = require=20 explanation. As they put it, =93given that the early branching points of = major=20 clades is an inevitable result of clade diversification, the alleged = phenomenon=20 of the phyla appearing early and remaining morphologically static is not = seen to=20 require particular explanation=94 (Budd & Jensen = 2000:253).

While=20 superficially plausible, perhaps, Budd and Jensen's attempt to explain = away the=20 Cambrian explosion begs crucial questions. Granted, as new characters = are added=20 to existing forms, novels morphology and greater morphological disparity = will=20 likely result. But what causes new characters to arise? And how does the = information necessary to produce new characters originate? Budd and = Jensen do=20 not specify. Nor can they say how derived the ancestral forms are likely = to have=20 been, and what processes, might have been sufficient to produce them. = Instead,=20 they simply assume the sufficiency of known neo-Darwinian mechanisms = (Budd &=20 Jensen 2000:288). Yet, as shown above, this assumption is now = problematic. In=20 any case, Budd and Jensen do not explain what causes the origination of=20 biological form and information.

Convergence and Teleological=20 Evolution

More recently, Conway Morris (2000, 2003c) has = suggested=20 another possible explanation based on the tendency for evolution to = converge on=20 the same structural forms during the history of life. Conway Morris = cites=20 numerous examples of organisms that possess very similar forms and = structures,=20 even though such structures are often built from different material = substrates=20 and arise (in ontogeny) by the expression of very different genes. Given = the=20 extreme improbability of the same structures arising by random mutation = and=20 selection in disparate phylogenies, Conway Morris argues that the = pervasiveness=20 of convergent structures suggests that evolution may be in some way = =93channeled=94=20 toward similar functional and/or structural endpoints. Such an = end-directed=20 understanding of evolution, he admits, raises the controversial prospect = of a=20 teleological or purposive element in the history of life. For this = reason, he=20 argues that the phenomenon of convergence has received less attention = than it=20 might have otherwise. Nevertheless, he argues that just as physicists = have=20 reopened the question of design in their discussions of anthropic = fine-tuning,=20 the ubiquity of convergent structures in the history of life has led = some=20 biologists (Denton 1998) to consider extending teleological thinking to = biology.=20 And, indeed, Conway Morris himself intimates that the evolutionary = process might=20 be =93underpinned by a purpose=94 (2000:8, 2003b:511).

Conway = Morris, of=20 course, considers this possibility in relation to a very specific aspect = of the=20 problem of organismal form, namely, the problem of explaining why the = same forms=20 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=20 causal question that has been addressed in this review? Could the notion = of=20 purposive design help provide a more adequate explanation for the origin = of=20 organismal form generally? Are there reasons to consider design as an=20 explanation for the origin of the biological information necessary to = produce=20 the higher taxa and their corresponding morphological = novelty?

The=20 remainder of this review will suggest that there are such reasons. In so = doing,=20 it may also help explain why the issue of teleology or design has = reemerged=20 within the scientific discussion of biological origins (Denton 1986, = 1998;=20 Thaxton et al. 1992; Kenyon & Mills 1996: Behe 1996, 2004; Dembski = 1998,=20 2002, 2004; Conway Morris 2000, 2003a, 2003b, Lonnig 2001; Lonnig & = Saedler=20 2002; Nelson & Wells 2003; Meyer 2003, 2004; Bradley 2004) and why = some=20 scientists and philosophers of science have considered teleological = explanations=20 for the origin of form and information despite strong methodological=20 prohibitions against design as a scientific hypothesis (Gillespie 1979, = Lenior=20 1982:4).

First, the possibility of design as an explanation = follows=20 logically from a consideration of the deficiencies of neo-Darwinism and = other=20 current theories as explanations for some of the more striking = =93appearances of=20 design=94 in biological systems. Neo-Darwinists such as Ayala (1994:5), = Dawkins=20 (1986:1), Mayr (1982:xi-xii) and Lewontin (1978) have long acknowledged = that=20 organisms appear to have been designed. Of course, neo-Darwinists assert = that=20 what Ayala (1994:5) calls the =93obvious design=94 of living things is = only apparent=20 since the selection/mutation mechanism can explain the origin of complex = form=20 and organization in living systems without an appeal to a designing = agent.=20 Indeed, neo-Darwinists affirm that mutation and selection--and perhaps = other=20 similarly undirected mechanisms--are fully sufficient to explain the = appearance=20 of design in biology. Self-organizational theorists and = punctuationalists modify=20 this claim, but affirm its essential tenet. Self-organization theorists = argue=20 that natural selection acting on self organizing order can explain the=20 complexity of living things--again, without any appeal to design.=20 Punctuationalists similarly envision natural selection acting on newly = arising=20 species with no actual design involved.

And clearly, the = neo-Darwinian=20 mechanism does explain many appearances of design, such as the = adaptation of=20 organisms to specialized environments that attracted the interest of = 19th=20 century biologists. More specifically, known microevolutionary processes = appear=20 quite sufficient to account for changes in the size of Galapagos finch = beaks=20 that have occurred in response to variations in annual rainfall and = available=20 food supplies (Weiner 1994, Grant 1999).

But does neo-Darwinism, = or any=20 other fully materialistic model, explain all appearances of design in = biology,=20 including the body plans and information that characterize living = systems?=20 Arguably, biological forms--such as the structure of a chambered = nautilus, the=20 organization of a trilobite, the functional integration of parts in an = eye or=20 molecular machine--attract our attention in part because the organized=20 complexity of such systems seems reminiscent of our own designs. Yet, = this=20 review has argued that neo-Darwinism does not adequately account for the = origin=20 of all appearances of design, especially if one considers animal body = plans, and=20 the information necessary to construct them, as especially striking = examples of=20 the appearance of design in living systems. Indeed, Dawkins (1995:11) = and Gates=20 (1996:228) have noted that genetic information bears an uncanny = resemblance to=20 computer software or machine code. For this reason, the presence of CSI = in=20 living organisms, and the discontinuous increases of CSI that occurred = during=20 events such as the Cambrian explosion, appears at least suggestive of=20 design.

Does neo-Darwinism or any other purely materialistic = model of=20 morphogenesis account for the origin of the genetic and other forms of = CSI=20 necessary to produce novel organismal form? If not, as this review has = argued,=20 could the emergence of novel information-rich genes, proteins, cell = types and=20 body plans have resulted from actual design, rather than a purposeless = process=20 that merely mimics the powers of a designing intelligence? The logic of=20 neo-Darwinism, with its specific claim to have accounted for the = appearance of=20 design, would itself seem to open the door to this possibility. Indeed, = the=20 historical formulation of Darwinism in dialectical opposition to the = design=20 hypothesis (Gillespie 1979), coupled with the neo-Darwinism's inability = to=20 account for many salient appearances of design including the emergence = of form=20 and information, would seem logically to reopen the possibility of = actual (as=20 opposed to apparent) design in the history of life.

A second = reason for=20 considering design as an explanation for these phenomena follows from = the=20 importance of explanatory power to scientific theory evaluation and from = a=20 consideration of the potential explanatory power of the design = hypothesis.=20 Studies in the methodology and philosophy of science have shown that = many=20 scientific theories, particularly in the historical sciences, are = formulated and=20 justified as inferences to the best explanation (Lipton 1991:32-88, = Brush=20 1989:1124-1129, Sober 2000:44). Historical scientists, in particular, = assess or=20 test competing hypotheses by evaluating which hypothesis would, if true, = provide=20 the best explanation for some set of relevant data (Meyer 1991, 2002; = Cleland=20 2001:987-989, 2002:474-496).¹⁰=20 Those with greater explanatory power are typically judged to be better, = more=20 probably true, theories. Darwin (1896:437) used this method of reasoning = in=20 defending his theory of universal common descent. Moreover, contemporary = studies=20 on the method of =93inference to the best explanation=94 have shown that = determining=20 which among a set of competing possible explanations constitutes the = best=20 depends upon judgments about the causal adequacy, or =93causal = powers,=94 of=20 competing explanatory entities (Lipton 1991:32-88). In the historical = sciences,=20 uniformitarian and/or actualistic (Gould 1965, Simpson 1970, Rutten = 1971,=20 Hooykaas 1975) canons of method suggest that judgments about causal = adequacy=20 should derive from our present knowledge of cause and effect = relationships. For=20 historical scientists, =93the present is the key to the past=94 means = that present=20 experience-based knowledge of cause and effect relationships typically = guides=20 the assessment of the plausibility of proposed causes of past = events.

Yet=20 it is precisely for this reason that current advocates of the design = hypothesis=20 want to reconsider design as an explanation for the origin of biological = form=20 and information. This review, and much of the literature it has = surveyed,=20 suggests that four of the most prominent models for explaining the = origin of=20 biological form fail to provide adequate causal explanations for the=20 discontinuous increases of CSI that are required to produce novel = morphologies.=20 Yet, we have repeated experience of rational and conscious agents--in = particular=20 ourselves--generating or causing increases in complex specified = information,=20 both in the form of sequence-specific lines of code and in the form of=20 hierarchically arranged systems of parts.

In the first place, = intelligent=20 human agents--in virtue of their rationality and consciousness--have=20 demonstrated the power to produce information in the form of linear=20 sequence-specific arrangements of characters. Indeed, experience affirms = that=20 information of this type routinely arises from the activity of = intelligent=20 agents. A computer user who traces the information on a screen back to = its=20 source invariably comes to a mind--that of a software engineer or = programmer. The information in a book or inscriptions ultimately derives = from a=20 writer or scribe--from a mental, rather than a strictly material, cause. = Our=20 experience-based knowledge of information-flow confirms that systems = with large=20 amounts of specified complexity (especially codes and languages) = invariably=20 originate from an intelligent source from a mind or personal agent. As = Quastler=20 (1964) put it, the =93creation of new information is habitually = associated with=20 conscious activity=94 (p. 16). Experience teaches this obvious=20 truth.

Further, the highly specified hierarchical arrangements of = parts=20 in animal body plans also suggest design, again because of our = experience=20 of the kinds of features and systems that designers can and do produce. = At every=20 level of the biological hierarchy, organisms require specified and = highly=20 improbable arrangements of lower-level constituents in order to maintain = their=20 form and function. Genes require specified arrangements of nucleotide = bases;=20 proteins require specified arrangements of amino acids; new cell types = require=20 specified arrangements of systems of proteins; body plans require = specialized=20 arrangements of cell types and organs. Organisms not only contain=20 information-rich components (such as proteins and genes), but they = comprise=20 information-rich arrangements of those components and the systems that = comprise=20 them. Yet we know, based on our present experience of cause and effect=20 relationships, that design engineers--possessing purposive intelligence = and=20 rationality--have the ability to produce information-rich hierarchies in = which=20 both individual modules and the arrangements of those modules exhibit = complexity=20 and specificity--information so defined. Individual transistors, = resistors, and=20 capacitors exhibit considerable complexity and specificity of design; at = a=20 higher level of organization, their specific arrangement within an = integrated=20 circuit represents additional information and reflects further design. = Conscious=20 and rational agents have, as part of their powers of purposive = intelligence, the=20 capacity to design information-rich parts and to organize those parts = into=20 functional information-rich systems and hierarchies. Further, we know of = no=20 other causal entity or process that has this capacity. Clearly, we have = good=20 reason to doubt that mutation and selection, self-organizational = processes or=20 laws of nature, can produce the information-rich components, systems, = and body=20 plans necessary to explain the origination of morphological novelty such = as that=20 which arises in the Cambrian period.

There is a third reason to = consider=20 purpose or design as an explanation for the origin of biological form = and=20 information: purposive agents have just those necessary powers that = natural=20 selection lacks as a condition of its causal adequacy. At several points = in the=20 previous analysis, we saw that natural selection lacked the ability to = generate=20 novel information precisely because it can only act after new = functional=20 CSI has arisen. Natural selection can favor new proteins, and genes, but = only=20 after they perform some function. The job of generating new functional = genes,=20 proteins and systems of proteins therefore falls entirely to random = mutations.=20 Yet without functional criteria to guide a search through the space of = possible=20 sequences, random variation is probabilistically doomed. What is needed = is not=20 just a source of variation (i.e., the freedom to search a space of=20 possibilities) or a mode of selection that can operate after the fact of = a=20 successful search, but instead a means of selection that (a) operates = during a=20 search--before success--and that (b) is guided by information about, or=20 knowledge of, a functional target.

Demonstration of this = requirement has=20 come from an unlikely quarter: genetic algorithms. Genetic algorithms = are=20 programs that allegedly simulate the creative power of mutation and = selection.=20 Dawkins and Kuppers, for example, have developed computer programs that=20 putatively simulate the production of genetic information by mutation = and=20 natural selection (Dawkins 1986:47-49, Kuppers 1987:355-369). = Nevertheless, as=20 shown elsewhere (Meyer 1998:127-128, 2003:247-248), these programs only = succeed=20 by the illicit expedient of providing the computer with a =93target = sequence=94 and=20 then treating relatively greater proximity to future function = (i.e., the=20 target sequence), not actual present function, as a selection criterion. = As=20 Berlinski (2000) has argued, genetic algorithms need something akin to a = =93forward looking memory=94 in order to succeed. Yet such foresighted = selection has=20 no analogue in nature. In biology, where differential survival depends = upon=20 maintaining function, selection cannot occur before new functional = sequences=20 arise. Natural selection lacks foresight.

What natural selection = lacks,=20 intelligent selection--purposive or goal-directed design--provides. = Rational=20 agents can arrange both matter and symbols with distant goals in mind. = In using=20 language, the human mind routinely =93finds=94 or generates highly = improbable=20 linguistic sequences to convey an intended or preconceived idea. = In the=20 process of thought, functional objectives precede and constrain the = selection of=20 words, sounds and symbols to generate functional (and indeed meaningful) = sequences from among a vast ensemble of meaningless alternative = combinations of=20 sound or symbol (Denton 1986:309-311). Similarly, the construction of = complex=20 technological objects and products, such as bridges, circuit boards, = engines and=20 software, result from the application of goal-directed constraints = (Polanyi=20 1967, 1968). Indeed, in all functionally integrated complex systems = where the=20 cause is known by experience or observation, design engineers or other=20 intelligent agents applied boundary constraints to limit possibilities = in order=20 to produce improbable forms, sequences or structures. Rational agents = have=20 repeatedly demonstrated the capacity to constrain the possible to = actualize=20 improbable but initially unrealized future functions. Repeated = experience=20 affirms that intelligent agents (minds) uniquely possess such causal=20 powers.

Analysis of the problem of the origin of biological = information,=20 therefore, exposes a deficiency in the causal powers of natural = selection that=20 corresponds precisely to powers that agents are uniquely known to = possess.=20 Intelligent agents have foresight. Such agents can select functional = goals=20 before they exist. They can devise or select material means to = accomplish=20 those ends from among an array of possibilities and then actualize those = goals=20 in accord with a preconceived design plan or set of functional = requirements.=20 Rational agents can constrain combinatorial space with distant outcomes = in mind.=20 The causal powers that natural selection lacks--almost by = definition--are=20 associated with the attributes of consciousness and rationality--with = purposive=20 intelligence. Thus, by invoking design to explain the origin of new = biological=20 information, contemporary design theorists are not positing an arbitrary = explanatory element unmotivated by a consideration of the evidence. = Instead,=20 they are positing an entity possessing precisely the attributes and = causal=20 powers that the phenomenon in question requires as a condition of its = production=20 and explanation.

Conclusion

An experience-based = analysis of=20 the causal powers of various explanatory hypotheses suggests purposive = or=20 intelligent design as a causally adequate--and perhaps the most causally = adequate--explanation for the origin of the complex specified = information=20 required to build the Cambrian animals and the novel forms they = represent. For=20 this reason, recent scientific interest in the design hypothesis is = unlikely to=20 abate as biologists continue to wrestle with the problem of the = origination of=20 biological form and the higher taxa.

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End Notes

¹ = Specifically, Gilbert et al. (1996) argued that changes in morphogenetic = fields=20 might produce large-scale changes in the developmental programs and, = ultimately,=20 body plans of organisms. Yet they offered no evidence that such = fields--if=20 indeed they exist--can be altered to produce advantageous variations in = body=20 plan, though this is a necessary condition of any successful causal = theory of=20 macroevolution.

2 If one takes the = fossil=20 record at face value and assumes that the Cambrian explosion took place = within a=20 relatively narrow 5-10 million year window, explaining the origin of the = information necessary to produce new proteins, for example, becomes more = acute=20 in part because mutation rates would not have been sufficient to = generate the=20 number of changes in the genome necessary to build the new proteins for = more=20 complex Cambrian animals (Ohno 1996:8475-8478). This review will argue = that,=20 even if one allows several hundred million years for the origin of the = metazoan,=20 significant probabilistic and other difficulties remain with the = neo-Darwinian=20 explanation of the origin of form and information.

³ As Crick put it, =93information means here the=20 precise determination of sequence, either of bases in the nucleic = acid or=20 on amino acid residues in the protein=94 (Crick 1958:144, = 153).

⁴ To solve this problem Ohno himself proposes the = existence=20 of a hypothetical ancestral form that possessed virtually all the = genetic=20 information necessary to produce the new body plans of the Cambrian = animals. He=20 asserts that this ancestor and its =93pananimalian genome=94 might have = arisen=20 several hundred million years before the Cambrian explosion. On this = view, each=20 of the different Cambrian animals would have possessed virtually = identical=20 genomes, albeit with considerable latent and unexpressed capacity in the = case of=20 each individual form (Ohno 1996:8475-8478). While this proposal might = help=20 explain the origin of the Cambrian animal forms by reference to = preexisting=20 genetic information, it does not solve, but instead merely displaces, = the=20 problem of the origin of the genetic information necessary to produce = these new=20 forms.

5 Some have suggested that = mutations=20 in =93master regulator=94 Hox genes might provide the raw material for = body plan=20 morphogenesis. Yet there are two problems with this proposal. First, Hox = gene=20 expression begins only after the foundation of the body plan has been=20 established in early embryogenesis. (Davidson 2001:66). Second, Hox = genes are=20 highly conserved across many disparate phyla and so cannot account for = the=20 morphological differences that exist between the phyla (Valentine=20 2004:88).

6 Notable differences in = the=20 developmental pathways of similar organisms have been observed. For = example,=20 congeneric species of sea urchins (from genus Heliocidaris) = exhibit=20 striking differences in their developmental pathways (Raff = 1999:110-121). Thus,=20 it might be argued that such differences show that early developmental = programs=20 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=20 differences in sea urchin development arose by mutation. Second, the = observed=20 differences in the developmental programs of different species of sea = urchins do=20 not result in new body plans, but instead in highly conserved = structures.=20 Despite differences in developmental patterns, the endpoints are the = same. Thus,=20 even if it can be assumed that mutations produced the differences in=20 developmental pathways, it must be acknowledged that such changes did = not result=20 in novel form.

7 Of course, many=20 post-translation processes of modification also play a role in producing = a=20 functional protein. Such processes make it impossible to predict a = protein's=20 final sequencing from its corresponding gene sequence alone (Sarkar=20 1996:199-202).

8 Erwin (2004:21), = although=20 friendly to the possibility of species selection, argues that Gould = provides=20 little evidence for its existence. =93The difficulty=94 writes Erwin of = species=20 selection, =93...is that we must rely on Gould's arguments for = theoretical=20 plausibility and sufficient relative frequency. Rarely is a mass of data = presented to justify and support Gould's conclusion.=94 Indeed, Gould = (2002)=20 himself admitted that species selection remains largely a hypothetical=20 construct: =93I freely admit that well-documented cases of species = selection do=20 not permeate the literature=94 (p. 710).

9=94I=20 do not deny either the wonder, or the powerful importance, of organized = adaptive=20 complexity. I recognize that we know no mechanism for the origin of such = organismal features other than conventional natural selection at the = organismic=20 level--for the sheer intricacy and elaboration of good biomechanical = design=20 surely precludes either random production, or incidental origin as a = side=20 consequence of active processes at other levels=94 (Gould 2002:710). = =93Thus, we do=20 not challenge the efficacy or the cardinal importance of organismal = selection.=20 As previously discussed, I fully agree with Dawkins (1986) and others = that one=20 cannot invoke a higher-level force like species selection to explain = 'things=20 that organisms do'--in particular, the stunning panoply of organismic=20 adaptations that has always motivated our sense of wonder about the = natural=20 world, and that Darwin (1859) described, in one of his most famous lines = (3), as=20 'that perfection of structure and coadaptation which most justly excites = our=20 admiration'=93 (Gould 2002:886).

10 Theories=20 in the historical sciences typically make claims about what happened in = the=20 past, or what happened in the past to cause particular events to occur = (Meyer=20 1991:57-72). For this reason, historical scientific theories are rarely = tested=20 by making predictions about what will occur under controlled laboratory=20 conditions (Cleland 2001:987, 2002:474-496). Instead, such theories are = usually=20 tested by comparing their explanatory power against that of their = competitors=20 with respect to already known facts. Even in the case in which = historical=20 theories make claims about past causes they usually do so on the basis = of=20 preexisting knowledge of cause and effect relationships. Nevertheless,=20 prediction may play a limited role in testing historical scientific = theories=20 since such theories may have implications as to what kind of evidence is = likely=20 to emerge in the future. For example, neo-Darwinism affirms that new = functional=20 sections of the genome arise by trial and error process of mutation and=20 subsequent selection. For this reason, historically many neo-Darwinists = expected=20 or predicted that the large non-coding regions of the genome--so-called = =93junk=20 DNA=94--would lack function altogether (Orgel & Crick 1980). On this = line of=20 thinking, the nonfunctional sections of the genome represent nature's = failed=20 experiments that remain in the genome as a kind of artifact of the past = activity=20 of the mutation and selection process. Advocates of the design = hypotheses on the=20 other hand, would have predicted that non-coding regions of the genome = might=20 well reveal hidden functions, not only because design theorists do not = think=20 that new genetic information arises by a trial and error process of = mutation and=20 selection, but also because designed systems are often functionally = polyvalent.=20 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=20 longer be said to make this claim in the form of a specifically = future-oriented=20 prediction. Instead, the design hypothesis might be said to gain = confirmation or=20 support from its ability to explain this now known evidence, albeit = after the=20 fact. Of course, neo Darwinists might also amend their original = prediction using=20 various auxiliary hypotheses to explain away the presence of newly = discovered=20 functions in the non-coding regions of DNA. In both cases, = considerations of=20 ex post facto explanatory power reemerge as central to assessing = and=20 testing competing historical theories.

Discovery Institute =97 Center for Science and = Culture
1511=20 Third Ave., Suite 808 =97 Seattle, WA 98101
206-292-0401 phone =97 = 206-682-5320=20 fax
email: cscinfo@discovery.org

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