The Origin of Biological Information and the
Higher Taxonomic CategoriesProceedings of the Biological
Society of WashingtonSeptember 29,
2004On August 4th, 2004 an
extensive review essay by Dr. Stephen C. Meyer, Director of Discovery
Institute's Center for Science & Culture appeared in the Proceedings of
the Biological Society of Washington (volume 117, no. 2, pp. 213-239). The
Proceedings is a peer-reviewed biology journal published at the National
Museum of Natural History at the Smithsonian Institution in Washington D.C.
In the article, entitled “The Origin of Biological Information and the
Higher Taxonomic Categories”, Dr. Meyer argues that no current materialistic
theory of evolution can account for the origin of the information necessary to
build novel animal forms. He proposes intelligent design as an alternative
explanation for the origin of biological information and the higher taxa.
Due to an unusual number of inquiries about the article and because the
article is presently not available on line elsewhere, Dr. Meyer, the copyright
holder, has decided to make the article available now in HTML format on this
website. (Off prints are also available from Discovery Institute by writing to
Keith Pennock at Kpennock@discovery.org).
PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON
The origin of biological information and the higher taxonomic
In a recent volume of the
Vienna Series in a Theoretical Biology (2003), Gerd B. Muller and Stuart Newman
argue that what they call the “origination of organismal form” remains an
unsolved problem. In making this claim, Muller and Newman (2003:3-10)
distinguish two distinct issues, namely, (1) the causes of form generation in
the individual organism during embryological development and (2) the causes
responsible for the production of novel organismal forms in the first place
during the history of life. To distinguish the latter case (phylogeny) from the
former (ontogeny), Muller and Newman use the term “origination” to designate the
causal processes by which biological form first arose during the evolution of
life. They insist that “the molecular mechanisms that bring about biological
form in modern day embryos should not be confused” with the causes responsible
for the origin (or “origination”) of novel biological forms during the history
of life (p.3). They further argue that we know more about the causes of
ontogenesis, due to advances in molecular biology, molecular genetics and
developmental biology, than we do about the causes of phylogenesis--the ultimate
origination of new biological forms during the remote past.
this claim, Muller and Newman are careful to affirm that evolutionary biology
has succeeded in explaining how preexisting forms diversify under the twin
influences of natural selection and variation of genetic traits. Sophisticated
mathematically-based models of population genetics have proven adequate for
mapping and understanding quantitative variability and populational changes in
organisms. Yet Muller and Newman insist that population genetics, and thus
evolutionary biology, has not identified a specifically causal explanation for
the origin of true morphological novelty during the history of life. Central to
their concern is what they see as the inadequacy of the variation of genetic
traits as a source of new form and structure. They note, following Darwin
himself, that the sources of new form and structure must precede the action of
natural selection (2003:3)--that selection must act on what already exists. Yet,
in their view, the “genocentricity” and “incrementalism” of the neo-Darwinian
mechanism has meant that an adequate source of new form and structure has yet to
be identified by theoretical biologists. Instead, Muller and Newman see the need
to identify epigenetic sources of morphological innovation during the evolution
of life. In the meantime, however, they insist neo-Darwinism lacks any “theory
of the generative” (p. 7).
As it happens, Muller and Newman are not alone
in this judgment. In the last decade or so a host of scientific essays and books
have questioned the efficacy of selection and mutation as a mechanism for
generating morphological novelty, as even a brief literature survey will
establish. Thomson (1992:107) expressed doubt that large-scale morphological
changes could accumulate via minor phenotypic changes at the population genetic
level. Miklos (1993:29) argued that neo-Darwinism fails to provide a mechanism
that can produce large-scale innovations in form and complexity. Gilbert et al.
(1996) attempted to develop a new theory of evolutionary mechanisms to
supplement classical neo-Darwinism, which, they argued, could not adequately
explain macroevolution. As they put it in a memorable summary of the situation:
“starting in the 1970s, many biologists began questioning its (neo-Darwinism's)
adequacy in explaining evolution. Genetics might be adequate for explaining
microevolution, but microevolutionary changes in gene frequency were not seen as
able to turn a reptile into a mammal or to convert a fish into an amphibian.
Microevolution looks at adaptations that concern the survival of the fittest,
not the arrival of the fittest. As Goodwin (1995) points out, 'the origin of
species--Darwin's problem--remains unsolved'“ (p. 361). Though Gilbert et al.
(1996) attempted to solve the problem of the origin of form by proposing a
greater role for developmental genetics within an otherwise neo-Darwinian
numerous recent authors have continued to raise questions about the adequacy of
that framework itself or about the problem of the origination of form generally
(Webster & Goodwin 1996; Shubin & Marshall 2000; Erwin 2000; Conway
Morris 2000, 2003b; Carroll 2000; Wagner 2001; Becker & Lonnig 2001; Stadler
et al. 2001; Lonnig & Saedler 2002; Wagner & Stadler 2003; Valentine
What lies behind this skepticism? Is it warranted? Is a
new and specifically causal theory needed to explain the origination of
This review will address these questions. It will do so
by analyzing the problem of the origination of organismal form (and the
corresponding emergence of higher taxa) from a particular theoretical
standpoint. Specifically, it will treat the problem of the origination of the
higher taxonomic groups as a manifestation of a deeper problem, namely, the
problem of the origin of the information (whether genetic or epigenetic) that,
as it will be argued, is necessary to generate morphological novelty.
order to perform this analysis, and to make it relevant and tractable to
systematists and paleontologists, this paper will examine a paradigmatic example
of the origin of biological form and information during the history of life: the
Cambrian explosion. During the Cambrian, many novel animal forms and body plans
(representing new phyla, subphyla and classes) arose in a geologically brief
period of time. The following information-based analysis of the Cambrian
explosion will support the claim of recent authors such as Muller and Newman
that the mechanism of selection and genetic mutation does not constitute an
adequate causal explanation of the origination of biological form in the higher
taxonomic groups. It will also suggest the need to explore other possible causal
factors for the origin of form and information during the evolution of life and
will examine some other possibilities that have been proposed.
The “Cambrian explosion” refers to the
geologically sudden appearance of many new animal body plans about 530 million
years ago. At this time, at least nineteen, and perhaps as many as thirty-five
phyla of forty total (Meyer et al. 2003), made their first appearance on earth
within a narrow five- to ten-million-year window of geologic time (Bowring et
al. 1993, 1998a:1, 1998b:40; Kerr 1993; Monastersky 1993; Aris-Brosou & Yang
2003). Many new subphyla, between 32 and 48 of 56 total (Meyer et al. 2003), and
classes of animals also arose at this time with representatives of these new
higher taxa manifesting significant morphological innovations. The Cambrian
explosion thus marked a major episode of morphogenesis in which many new and
disparate organismal forms arose in a geologically brief period of
To say that the fauna of the Cambrian period appeared in a
geologically sudden manner also implies the absence of clear transitional
intermediate forms connecting Cambrian animals with simpler pre-Cambrian forms.
And, indeed, in almost all cases, the Cambrian animals have no clear
morphological antecedents in earlier Vendian or Precambrian fauna (Miklos 1993,
Erwin et al. 1997:132, Steiner & Reitner 2001, Conway Morris 2003b:510,
Valentine et al. 2003:519-520). Further, several recent discoveries and analyses
suggest that these morphological gaps may not be merely an artifact of
incomplete sampling of the fossil record (Foote 1997, Foote et al. 1999, Benton
& Ayala 2003, Meyer et al. 2003), suggesting that the fossil record is at
least approximately reliable (Conway Morris 2003b:505).
As a result,
debate now exists about the extent to which this pattern of evidence comports
with a strictly monophyletic view of evolution (Conway Morris 1998a, 2003a,
2003b:510; Willmer 1990, 2003). Further, among those who accept a monophyletic
view of the history of life, debate exists about whether to privilege fossil or
molecular data and analyses. Those who think the fossil data provide a more
reliable picture of the origin of the Metazoan tend to think these animals arose
relatively quickly--that the Cambrian explosion had a “short fuse.” (Conway
Morris 2003b:505-506, Valentine & Jablonski 2003). Some (Wray et al. 1996),
but not all (Ayala et al. 1998), who think that molecular phylogenies establish
reliable divergence times from pre-Cambrian ancestors think that the Cambrian
animals evolved over a very long period of time--that the Cambrian explosion had
a “long fuse.” This review will not address these questions of historical
pattern. Instead, it will analyze whether the neo-Darwinian process of mutation
and selection, or other processes of evolutionary change, can generate the form
and information necessary to produce the animals that arise in the Cambrian.
This analysis will, for the most part, 2
therefore, not depend upon assumptions of either a long or short fuse for the
Cambrian explosion, or upon a monophyletic or polyphyletic view of the early
history of life.
Defining Biological Form and
Form, like life itself, is easy to recognize but often
hard to define precisely. Yet, a reasonable working definition of form will
suffice for our present purposes. Form can be defined as the four-dimensional
topological relations of anatomical parts. This means that one can understand
form as a unified arrangement of body parts or material components in a distinct
shape or pattern (topology)--one that exists in three spatial dimensions and
which arises in time during ontogeny.
Insofar as any particular
biological form constitutes something like a distinct arrangement of constituent
body parts, form can be seen as arising from constraints that limit the possible
arrangements of matter. Specifically, organismal form arises (both in phylogeny
and ontogeny) as possible arrangements of material parts are constrained to
establish a specific or particular arrangement with an identifiable three
dimensional topography--one that we would recognize as a particular protein,
cell type, organ, body plan or organism. A particular “form,” therefore,
represents a highly specific and constrained arrangement of material components
(among a much larger set of possible arrangements).
in this way suggests a connection to the notion of information in its most
theoretically general sense. When Shannon (1948) first developed a mathematical
theory of information he equated the amount of information transmitted with the
amount of uncertainty reduced or eliminated in a series of symbols or
characters. Information, in Shannon's theory, is thus imparted as some options
are excluded and others are actualized. The greater the number of options
excluded, the greater the amount of information conveyed. Further, constraining
a set of possible material arrangements by whatever process or means involves
excluding some options and actualizing others. Thus, to constrain a set of
possible material states is to generate information in Shannon's sense. It
follows that the constraints that produce biological form also imparted
information. Or conversely, one might say that producing organismal form
by definition requires the generation of information.
Shannon information theory, the amount of information in a system is also
inversely related to the probability of the arrangement of constituents in a
system or the characters along a communication channel (Shannon 1948). The more
improbable (or complex) the arrangement, the more Shannon information, or
information-carrying capacity, a string or system possesses.
1960s, mathematical biologists have realized that Shannon's theory could be
applied to the analysis of DNA and proteins to measure the information-carrying
capacity of these macromolecules. Since DNA contains the assembly instructions
for building proteins, the information-processing system in the cell represents
a kind of communication channel (Yockey 1992:110). Further, DNA conveys
information via specifically arranged sequences of nucleotide bases. Since each
of the four bases has a roughly equal chance of occurring at each site along the
spine of the DNA molecule, biologists can calculate the probability, and thus
the information-carrying capacity, of any particular sequence n bases
The ease with which information theory applies to molecular biology
has created confusion about the type of information that DNA and proteins
possess. Sequences of nucleotide bases in DNA, or amino acids in a protein, are
highly improbable and thus have large information-carrying capacities. But, like
meaningful sentences or lines of computer code, genes and proteins are also
specified with respect to function. Just as the meaning of a sentence
depends upon the specific arrangement of the letters in a sentence, so too does
the function of a gene sequence depend upon the specific arrangement of the
nucleotide bases in a gene. Thus, molecular biologists beginning with Crick
equated information not only with complexity but also with “specificity,”
where “specificity” or “specified” has meant “necessary to function” (Crick
1958:144, 153; Sarkar, 1996:191).3
Molecular biologists such as Monod and Crick understood biological
information--the information stored in DNA and proteins--as something more than
mere complexity (or improbability). Their notion of information associated both
biochemical contingency and combinatorial complexity with DNA sequences
(allowing DNA's carrying capacity to be calculated), but it also affirmed that
sequences of nucleotides and amino acids in functioning macromolecules possessed
a high degree of specificity relative to the maintenance of cellular
The ease with which information theory applies to molecular
biology has also created confusion about the location of information in
organisms. Perhaps because the information carrying capacity of the gene could
be so easily measured, it has been easy to treat DNA, RNA and proteins as the
sole repositories of biological information. Neo-Darwinists in particular have
assumed that the origination of biological form could be explained by recourse
to processes of genetic variation and mutation alone (Levinton 1988:485). Yet if
one understands organismal form as resulting from constraints on the possible
arrangements of matter at many levels in the biological hierarchy--from genes
and proteins to cell types and tissues to organs and body plans--then clearly
biological organisms exhibit many levels of information-rich
Thus, we can pose a question, not only about the origin of
genetic information, but also about the origin of the information necessary to
generate form and structure at levels higher than that present in individual
proteins. We must also ask about the origin of the “specified complexity,” as
opposed to mere complexity, that characterizes the new genes, proteins, cell
types and body plans that arose in the Cambrian explosion. Dembski (2002) has
used the term “complex specified information” (CSI) as a synonym for “specified
complexity” to help distinguish functional biological information from mere
Shannon information--that is, specified complexity from mere complexity. This
review will use this term as well.
The Cambrian Information
The Cambrian explosion represents a remarkable jump in the
specified complexity or “complex specified information” (CSI) of the biological
world. For over three billions years, the biological realm included little more
than bacteria and algae (Brocks et al. 1999). Then, beginning about 570-565
million years ago (mya), the first complex multicellular organisms appeared in
the rock strata, including sponges, cnidarians, and the peculiar Ediacaran biota
(Grotzinger et al. 1995). Forty million years later, the Cambrian explosion
occurred (Bowring et al. 1993). The emergence of the Ediacaran biota (570 mya),
and then to a much greater extent the Cambrian explosion (530 mya), represented
steep climbs up the biological complexity gradient.
One way to estimate
the amount of new CSI that appeared with the Cambrian animals is to count the
number of new cell types that emerged with them (Valentine 1995:91-93). Studies
of modern animals suggest that the sponges that appeared in the late
Precambrian, for example, would have required five cell types, whereas the more
complex animals that appeared in the Cambrian (e.g., arthropods) would have
required fifty or more cell types. Functionally more complex animals require
more cell types to perform their more diverse functions. New cell types require
many new and specialized proteins. New proteins, in turn, require new genetic
information. Thus an increase in the number of cell types implies (at a minimum)
a considerable increase in the amount of specified genetic information.
Molecular biologists have recently estimated that a minimally complex
single-celled organism would require between 318 and 562 kilobase pairs of DNA
to produce the proteins necessary to maintain life (Koonin 2000). More complex
single cells might require upward of a million base pairs. Yet to build the
proteins necessary to sustain a complex arthropod such as a trilobite would
require orders of magnitude more coding instructions. The genome size of a
modern arthropod, the fruitfly Drosophila melanogaster, is approximately
180 million base pairs (Gerhart & Kirschner 1997:121, Adams et al. 2000).
Transitions from a single cell to colonies of cells to complex animals represent
significant (and, in principle, measurable) increases in CSI.
new animal from a single-celled organism requires a vast amount of new genetic
information. It also requires a way of arranging gene products--proteins--into
higher levels of organization. New proteins are required to service new cell
types. But new proteins must be organized into new systems within the cell; new
cell types must be organized into new tissues, organs, and body parts. These, in
turn, must be organized to form body plans. New animals, therefore, embody
hierarchically organized systems of lower-level parts within a functional whole.
Such hierarchical organization itself represents a type of information, since
body plans comprise both highly improbable and functionally specified
arrangements of lower-level parts. The specified complexity of new body plans
requires explanation in any account of the Cambrian explosion.
neo-Darwinism explain the discontinuous increase in CSI that appears in the
Cambrian explosion--either in the form of new genetic information or in the form
of hierarchically organized systems of parts? We will now examine the two parts
of this question.
Novel Genes and Proteins
and mathematicians have questioned the ability of mutation and selection to
generate information in the form of novel genes and proteins. Such skepticism
often derives from consideration of the extreme improbability (and specificity)
of functional genes and proteins.
A typical gene contains over one
thousand precisely arranged bases. For any specific arrangement of four
nucleotide bases of length n, there is a corresponding number of possible
arrangements of bases, 4n. For any protein, there are
20n possible arrangements of protein-forming amino acids. A
gene 999 bases in length represents one of 4999 possible nucleotide
sequences; a protein of 333 amino acids is one of 20333
Since the 1960s, some biologists have thought functional
proteins to be rare among the set of possible amino acid sequences. Some have
used an analogy with human language to illustrate why this should be the case.
Denton (1986, 309-311), for example, has shown that meaningful words and
sentences are extremely rare among the set of possible combinations of English
letters, especially as sequence length grows. (The ratio of meaningful 12-letter
words to 12-letter sequences is 1/1014, the ratio of 100-letter
sentences to possible 100-letter strings is 1/10100.) Further, Denton shows that
most meaningful sentences are highly isolated from one another in the
space of possible combinations, so that random substitutions of letters will,
after a very few changes, inevitably degrade meaning. Apart from a few closely
clustered sentences accessible by random substitution, the overwhelming majority
of meaningful sentences lie, probabilistically speaking, beyond the reach of
Denton (1986:301-324) and others have argued that similar
constraints apply to genes and proteins. They have questioned whether an
undirected search via mutation and selection would have a reasonable chance of
locating new islands of function--representing fundamentally new genes or
proteins--within the time available (Eden 1967, Shutzenberger 1967, Lovtrup
1979). Some have also argued that alterations in sequencing would likely result
in loss of protein function before fundamentally new function could arise (Eden
1967, Denton 1986). Nevertheless, neither the extent to which genes and proteins
are sensitive to functional loss as a result of sequence change, nor the extent
to which functional proteins are isolated within sequence space, has been fully
Recently, experiments in molecular biology have shed light on
these questions. A variety of mutagenesis techniques have shown that proteins
(and thus the genes that produce them) are indeed highly specified relative to
biological function (Bowie & Sauer 1989, Reidhaar-Olson & Sauer 1990,
Taylor et al. 2001). Mutagenesis research tests the sensitivity of proteins
(and, by implication, DNA) to functional loss as a result of alterations in
sequencing. Studies of proteins have long shown that amino acid residues at many
active positions cannot vary without functional loss (Perutz & Lehmann
1968). More recent protein studies (often using mutagenesis experiments) have
shown that functional requirements place significant constraints on sequencing
even at non-active site positions (Bowie & Sauer 1989, Reidhaar-Olson &
Sauer 1990, Chothia et al. 1998, Axe 2000, Taylor et al. 2001). In particular,
Axe (2000) has shown that multiple as opposed to single position amino acid
substitutions inevitably result in loss of protein function, even when these
changes occur at sites that allow variation when altered in isolation.
Cumulatively, these constraints imply that proteins are highly sensitive to
functional loss as a result of alterations in sequencing, and that functional
proteins represent highly isolated and improbable arrangements of amino acids
-arrangements that are far more improbable, in fact, than would be likely to
arise by chance alone in the time available (Reidhaar-Olson & Sauer 1990;
Behe 1992; Kauffman 1995:44; Dembski 1998:175-223; Axe 2000, 2004). (See below
the discussion of the neutral theory of evolution for a precise quantitative
Of course, neo-Darwinists do not envision a completely
random search through the set of all possible nucleotide sequences--so-called
“sequence space.” They envision natural selection acting to preserve small
advantageous variations in genetic sequences and their corresponding protein
products. Dawkins (1996), for example, likens an organism to a high mountain
peak. He compares climbing the sheer precipice up the front side of the mountain
to building a new organism by chance. He acknowledges that his approach up
“Mount Improbable” will not succeed. Nevertheless, he suggests that there is a
gradual slope up the backside of the mountain that could be climbed in small
incremental steps. In his analogy, the backside climb up “Mount Improbable”
corresponds to the process of natural selection acting on random changes in the
genetic text. What chance alone cannot accomplish blindly or in one leap,
selection (acting on mutations) can accomplish through the cumulative effect of
many slight successive steps.
Yet the extreme specificity and complexity
of proteins presents a difficulty, not only for the chance origin of specified
biological information (i.e., for random mutations acting alone), but also for
selection and mutation acting in concert. Indeed, mutagenesis experiments cast
doubt on each of the two scenarios by which neo-Darwinists envisioned new
information arising from the mutation/selection mechanism (for review, see
Lonnig 2001). For neo-Darwinism, new functional genes either arise from
non-coding sections in the genome or from preexisting genes. Both scenarios are
In the first scenario, neo-Darwinists envision new genetic
information arising from those sections of the genetic text that can presumably
vary freely without consequence to the organism. According to this scenario,
non-coding sections of the genome, or duplicated sections of coding regions, can
experience a protracted period of “neutral evolution” (Kimura 1983) during which
alterations in nucleotide sequences have no discernible effect on the function
of the organism. Eventually, however, a new gene sequence will arise that can
code for a novel protein. At that point, natural selection can favor the new
gene and its functional protein product, thus securing the preservation and
heritability of both.
This scenario has the advantage of allowing the
genome to vary through many generations, as mutations “search” the space of
possible base sequences. The scenario has an overriding problem, however: the
size of the combinatorial space (i.e., the number of possible amino acid
sequences) and the extreme rarity and isolation of the functional sequences
within that space of possibilities. Since natural selection can do nothing to
help generate new functional sequences, but rather can only preserve such
sequences once they have arisen, chance alone--random variation--must do the
work of information generation--that is, of finding the exceedingly rare
functional sequences within the set of combinatorial possibilities. Yet the
probability of randomly assembling (or “finding,” in the previous sense) a
functional sequence is extremely small.
Cassette mutagenesis experiments
performed during the early 1990s suggest that the probability of attaining (at
random) the correct sequencing for a short protein 100 amino acids long is about
1 in 1065 (Reidhaar-Olson & Sauer 1990, Behe 1992:65-69). This
result agreed closely with earlier calculations that Yockey (1978) had performed
based upon the known sequence variability of cytochrome c in different species
and other theoretical considerations. More recent mutagenesis research has
provided additional support for the conclusion that functional proteins are
exceedingly rare among possible amino acid sequences (Axe 2000, 2004). Axe
(2004) has performed site directed mutagenesis experiments on a 150-residue
protein-folding domain within a B-lactamase enzyme. His experimental method
improves upon earlier mutagenesis techniques and corrects for several sources of
possible estimation error inherent in them. On the basis of these experiments,
Axe has estimated the ratio of (a) proteins of typical size (150 residues) that
perform a specified function via any folded structure to (b) the whole set of
possible amino acids sequences of that size. Based on his experiments, Axe has
estimated his ratio to be 1 to 1077. Thus, the probability of finding
a functional protein among the possible amino acid sequences corresponding to a
150-residue protein is similarly 1 in 1077.
considerations imply additional improbabilities. First, new Cambrian animals
would require proteins much longer than 100 residues to perform many necessary
specialized functions. Ohno (1996) has noted that Cambrian animals would have
required complex proteins such as lysyl oxidase in order to support their stout
body structures. Lysyl oxidase molecules in extant organisms comprise over 400
amino acids. These molecules are both highly complex (non-repetitive) and
functionally specified. Reasonable extrapolation from mutagenesis experiments
done on shorter protein molecules suggests that the probability of producing
functionally sequenced proteins of this length at random is so small as to make
appeals to chance absurd, even granting the duration of the entire universe.
(See Dembski 1998:175-223 for a rigorous calculation of this “Universal
Probability Bound”; See also Axe 2004.) Yet, second, fossil data (Bowring et al.
1993, 1998a:1, 1998b:40; Kerr 1993; Monatersky 1993), and even molecular
analyses supporting deep divergence (Wray et al. 1996), suggest that the
duration of the Cambrian explosion (between 5-10 x 106 and, at most,
7 x 107 years) is far smaller than that of the entire universe (1.3-2
x 1010 years). Third, DNA mutation rates are far too low to generate
the novel genes and proteins necessary to building the Cambrian animals, given
the most probable duration of the explosion as determined by fossil studies
(Conway Morris 1998b). As Ohno (1996:8475) notes, even a mutation rate of
10-9 per base pair per year results in only a 1% change in the
sequence of a given section of DNA in 10 million years. Thus, he argues that
mutational divergence of preexisting genes cannot explain the origin of the
Cambrian forms in that time.4
selection/mutation mechanism faces another probabilistic obstacle. The animals
that arise in the Cambrian exhibit structures that would have required many new
types of cells, each of which would have required many novel proteins to
perform their specialized functions. Further, new cell types require
Asystems of proteins that must, as a condition of functioning, act in
close coordination with one another. The unit of selection in such systems
ascends to the system as a whole. Natural selection selects for functional
advantage. But new cell types require whole systems of proteins to perform their
distinctive functions. In such cases, natural selection cannot contribute to the
process of information generation until after the information necessary
to build the requisite system of proteins has arisen. Thus random
variations must, again, do the work of information generation--and now not
simply for one protein, but for many proteins arising at nearly the same time.
Yet the odds of this occurring by chance alone are, of course, far smaller than
the odds of the chance origin of a single gene or protein--so small in fact as
to render the chance origin of the genetic information necessary to build a new
cell type (a necessary but not sufficient condition of building a new body plan)
problematic given even the most optimistic estimates for the duration of the
Dawkins (1986:139) has noted that scientific theories
can rely on only so much “luck” before they cease to be credible. The neutral
theory of evolution, which, by its own logic, prevents natural selection from
playing a role in generating genetic information until after the fact, relies on
entirely too much luck. The sensitivity of proteins to functional loss, the need
for long proteins to build new cell types and animals, the need for whole new
systems of proteins to service new cell types, the probable brevity of
the Cambrian explosion relative to mutation rates--all suggest the immense
improbability (and implausibility) of any scenario for the origination of
Cambrian genetic information that relies upon random variation alone unassisted
by natural selection.
Yet the neutral theory requires novel genes and
proteins to arise--essentially--by random mutation alone. Adaptive advantage
accrues after the generation of new functional genes and proteins. Thus,
natural selection cannot play a role until new information-bearing
molecules have independently arisen. Thus neutral theorists envisioned the need
to scale the steep face of a Dawkins-style precipice of which there is no
gradually sloping backside--a situation that, by Dawkins' own logic, is
In the second scenario, neo-Darwinists
envisioned novel genes and proteins arising by numerous successive mutations in
the preexisting genetic text that codes for proteins. To adapt Dawkins's
metaphor, this scenario envisions gradually climbing down one functional peak
and then ascending another. Yet mutagenesis experiments again suggest a
difficulty. Recent experiments show that, even when exploring a region of
sequence space populated by proteins of a single fold and function, most
multiple-position changes quickly lead to loss of function (Axe 2000). Yet to
turn one protein into another with a completely novel structure and function
requires specified changes at many sites. Indeed, the number of changes
necessary to produce a new protein greatly exceeds the number of changes that
will typically produce functional losses. Given this, the probability of
escaping total functional loss during a random search for the changes needed to
produce a new function is extremely small--and this probability diminishes
exponentially with each additional requisite change (Axe 2000). Thus, Axe's
results imply that, in all probability, random searches for novel proteins
(through sequence space) will result in functional loss long before any novel
functional protein will emerge.
Blanco et al. have come to a similar
conclusion. Using directed mutagenesis, they have determined that residues in
both the hydrophobic core and on the surface of the protein play essential roles
in determining protein structure. By sampling intermediate sequences between two
naturally occurring sequences that adopt different folds, they found that the
intermediate sequences “lack a well defined three-dimensional structure.” Thus,
they conclude that it is unlikely that a new protein fold via a series of folded
intermediates sequences (Blanco et al. 1999:741).
Thus, although this
second neo-Darwinian scenario has the advantage of starting with functional
genes and proteins, it also has a lethal disadvantage: any process of random
mutation or rearrangement in the genome would in all probability generate
nonfunctional intermediate sequences before fundamentally new functional genes
or proteins would arise. Clearly, nonfunctional intermediate sequences confer no
survival advantage on their host organisms. Natural selection favors only
functional advantage. It cannot select or favor nucleotide sequences or
polypeptide chains that do not yet perform biological functions, and still less
will it favor sequences that efface or destroy preexisting
Evolving genes and proteins will range through a series of
nonfunctional intermediate sequences that natural selection will not favor or
preserve but will, in all probability, eliminate (Blanco et al. 1999, Axe 2000).
When this happens, selection-driven evolution will cease. At this point, neutral
evolution of the genome (unhinged from selective pressure) may ensue, but, as we
have seen, such a process must overcome immense probabilistic hurdles, even
granting cosmic time.
Thus, whether one envisions the evolutionary
process beginning with a noncoding region of the genome or a preexisting
functional gene, the functional specificity and complexity of proteins impose
very stringent limitations on the efficacy of mutation and selection. In the
first case, function must arise first, before natural selection can act to favor
a novel variation. In the second case, function must be continuously maintained
in order to prevent deleterious (or lethal) consequences to the organism and to
allow further evolution. Yet the complexity and functional specificity of
proteins implies that both these conditions will be extremely difficult to meet.
Therefore, the neo-Darwinian mechanism appears to be inadequate to generate the
new information present in the novel genes and proteins that arise with the
Novel Body Plans
The problems with the
neo-Darwinian mechanism run deeper still. In order to explain the origin of the
Cambrian animals, one must account not only for new proteins and cell types, but
also for the origin of new body plans. Within the past decade, developmental
biology has dramatically advanced our understanding of how body plans are built
during ontogeny. In the process, it has also uncovered a profound difficulty for
Significant morphological change in organisms requires
attention to timing. Mutations in genes that are expressed late in the
development of an organism will not affect the body plan. Mutations expressed
early in development, however, could conceivably produce significant
morphological change (Arthur 1997:21). Thus, events expressed early in the
development of organisms have the only realistic chance of producing large-scale
macroevolutionary change (Thomson 1992). As John and Miklos (1988:309) explain,
macroevolutionary change requires alterations in the very early stages of
Yet recent studies in developmental biology make clear that
mutations expressed early in development typically have deleterious effects
(Arthur 1997:21). For example, when early-acting body plan molecules, or
morphogens such as bicoid (which helps to set up the anterior-posterior
head-to-tail axis in Drosophila), are perturbed, development shuts down
(Nusslein-Volhard & Wieschaus 1980, Lawrence & Struhl 1996, Muller &
The resulting embryos die. Moreover, there is a good reason for this. If an
engineer modifies the length of the piston rods in an internal combustion engine
without modifying the crankshaft accordingly, the engine won't start. Similarly,
processes of development are tightly integrated spatially and temporally such
that changes early in development will require a host of other coordinated
changes in separate but functionally interrelated developmental processes
downstream. For this reason, mutations will be much more likely to be deadly if
they disrupt a functionally deeply-embedded structure such as a spinal column
than if they affect more isolated anatomical features such as fingers (Kauffman
This problem has led to what McDonald (1983) has called “a
great Darwinian paradox” (p. 93). McDonald notes that genes that are observed to
vary within natural populations do not lead to major adaptive changes, while
genes that could cause major changes--the very stuff of
macroevolution--apparently do not vary. In other words, mutations of the kind
that macroevolution doesn't need (namely, viable genetic mutations in DNA
expressed late in development) do occur, but those that it does need (namely,
beneficial body plan mutations expressed early in development) apparently don't
According to Darwin (1859:108) natural selection cannot act until favorable
variations arise in a population. Yet there is no evidence from developmental
genetics that the kind of variations required by neo-Darwinism--namely,
favorable body plan mutations--ever occur.
Developmental biology has
raised another formidable problem for the mutation/selection mechanism.
Embryological evidence has long shown that DNA does not wholly determine
morphological form (Goodwin 1985, Nijhout 1990, Sapp 1987, Muller & Newman
2003), suggesting that mutations in DNA alone cannot account for the
morphological changes required to build a new body plan.
DNA helps direct
It also helps to regulate the timing and expression of the synthesis of various
proteins within cells. Yet, DNA alone does not determine how individual proteins
assemble themselves into larger systems of proteins; still less does it solely
determine how cell types, tissue types, and organs arrange themselves into body
plans (Harold 1995:2774, Moss 2004). Instead, other factors--such as the
three-dimensional structure and organization of the cell membrane and
cytoskeleton and the spatial architecture of the fertilized egg--play important
roles in determining body plan formation during embryogenesis.
example, the structure and location of the cytoskeleton influence the patterning
of embryos. Arrays of microtubules help to distribute the essential proteins
used during development to their correct locations in the cell. Of course,
microtubules themselves are made of many protein subunits. Nevertheless, like
bricks that can be used to assemble many different structures, the tubulin
subunits in the cell's microtubules are identical to one another. Thus, neither
the tubulin subunits nor the genes that produce them account for the different
shape of microtubule arrays that distinguish different kinds of embryos and
developmental pathways. Instead, the structure of the microtubule array itself
is determined by the location and arrangement of its subunits, not the
properties of the subunits themselves. For this reason, it is not possible to
predict the structure of the cytoskeleton of the cell from the characteristics
of the protein constituents that form that structure (Harold
Two analogies may help further clarify the point. At a
building site, builders will make use of many materials: lumber, wires, nails,
drywall, piping, and windows. Yet building materials do not determine the floor
plan of the house, or the arrangement of houses in a neighborhood. Similarly,
electronic circuits are composed of many components, such as resistors,
capacitors, and transistors. But such lower-level components do not determine
their own arrangement in an integrated circuit. Biological symptoms also depend
on hierarchical arrangements of parts. Genes and proteins are made from simple
building blocks--nucleotide bases and amino acids--arranged in specific ways.
Cell types are made of, among other things, systems of specialized proteins.
Organs are made of specialized arrangements of cell types and tissues. And body
plans comprise specific arrangements of specialized organs. Yet, clearly, the
properties of individual proteins (or, indeed, the lower-level parts in the
hierarchy generally) do not fully determine the organization of the higher-level
structures and organizational patterns (Harold 2001:125). It follows that the
genetic information that codes for proteins does not determine these
higher-level structures either.
These considerations pose another
challenge to the sufficiency of the neo-Darwinian mechanism. Neo-Darwinism seeks
to explain the origin of new information, form, and structure as a result of
selection acting on randomly arising variation at a very low level within the
biological hierarchy, namely, within the genetic text. Yet major morphological
innovations depend on a specificity of arrangement at a much higher level of the
organizational hierarchy, a level that DNA alone does not determine. Yet if DNA
is not wholly responsible for body plan morphogenesis, then DNA sequences can
mutate indefinitely, without regard to realistic probabilistic limits, and still
not produce a new body plan. Thus, the mechanism of natural selection acting on
random mutations in DNA cannot in principle generate novel body plans,
including those that first arose in the Cambrian explosion.
Of course, it
could be argued that, while many single proteins do not by themselves determine
cellular structures and/or body plans, proteins acting in concert with other
proteins or suites of proteins could determine such higher-level form. For
example, it might be pointed out that the tubulin subunits (cited above) are
assembled by other helper proteins--gene products--called Microtubule Associated
Proteins (MAPS). This might seem to suggest that genes and gene products alone
do suffice to determine the development of the three-dimensional structure of
Yet MAPS, and indeed many other necessary proteins, are
only part of the story. The location of specified target sites on the interior
of the cell membrane also helps to determine the shape of the cytoskeleton.
Similarly, so does the position and structure of the centrosome which nucleates
the microtubules that form the cytoskeleton. While both the membrane targets and
the centrosomes are made of proteins, the location and form of these structures
is not wholly determined by the proteins that form them. Indeed, centrosome
structure and membrane patterns as a whole convey three-dimensional
structural information that helps determine the structure of the cytoskeleton
and the location of its subunits (McNiven & Porter 1992:313-329). Moreover,
the centrioles that compose the centrosomes replicate independently of DNA
replication (Lange et al. 2000:235-249, Marshall & Rosenbaum 2000:187-205).
The daughter centriole receives its form from the overall structure of the
mother centriole, not from the individual gene products that constitute it
(Lange et al. 2000). In ciliates, microsurgery on cell membranes can produce
heritable changes in membrane patterns, even though the DNA of the ciliates has
not been altered (Sonneborn 1970:1-13, Frankel 1980:607-623; Nanney
1983:163-170). This suggests that membrane patterns (as opposed to membrane
constituents) are impressed directly on daughter cells. In both cases, form is
transmitted from parent three-dimensional structures to daughter
three-dimensional structures directly and is not wholly contained in constituent
proteins or genetic information (Moss 2004).
Thus, in each new
generation, the form and structure of the cell arises as the result of
both gene products and preexisting three-dimensional structure and
organization. Cellular structures are built from proteins, but proteins find
their way to correct locations in part because of preexisting three-dimensional
patterns and organization inherent in cellular structures. Preexisting
three-dimensional form present in the preceding generation (whether inherent in
the cell membrane, the centrosomes, the cytoskeleton or other features of the
fertilized egg) contributes to the production of form in the next generation.
Neither structural proteins alone, nor the genes that code for them, are
sufficient to determine the three-dimensional shape and structure of the
entities they form. Gene products provide necessary, but not sufficient
conditions, for the development of three-dimensional structure within cells,
organs and body plans (Harold 1995:2767). But if this is so, then natural
selection acting on genetic variation alone cannot produce the new forms that
arise in history of life.
course, neo-Darwinism is not the only evolutionary theory for explaining the
origin of novel biological form. Kauffman (1995) doubts the efficacy of the
mutation/selection mechanism. Nevertheless, he has advanced a
self-organizational theory to account for the emergence of new form, and
presumably the information necessary to generate it. Whereas neo-Darwinism
attempts to explain new form as the consequence of selection acting on random
mutation, Kauffman suggests that selection acts, not mainly on random
variations, but on emergent patterns of order that self-organize via the laws of
Kauffman (1995:47-92) illustrates how this might work with
various model systems in a computer environment. In one, he conceives a system
of buttons connected by strings. Buttons represent novel genes or gene products;
strings represent the law-like forces of interaction that obtain between gene
products-i.e., proteins. Kauffman suggests that when the complexity of the
system (as represented by the number of buttons and strings) reaches a critical
threshold, new modes of organization can arise in the system “for free”--that
is, naturally and spontaneously--after the manner of a phase transition in
Another model that Kauffman develops is a system of
interconnected lights. Each light can flash in a variety of states--on, off,
twinkling, etc. Since there is more than one possible state for each light, and
many lights, there are a vast number of possible states that the system can
adopt. Further, in his system, rules determine how past states will influence
future states. Kauffman asserts that, as a result of these rules, the system
will, if properly tuned, eventually produce a kind of order in which a few basic
patterns of light activity recur with greater-than-random frequency. Since these
actual patterns of light activity represent a small portion of the total number
of possible states in which the system can reside, Kauffman seems to imply that
self-organizational laws might similarly result in highly improbable biological
outcomes--perhaps even sequences (of bases or amino acids) within a much larger
sequence space of possibilities.
Do these simulations of
self-organizational processes accurately model the origin of novel genetic
information? It is hard to think so.
First, in both examples, Kauffman
presupposes but does not explain significant sources of preexisting information.
In his buttons-and-strings system, the buttons represent proteins, themselves
packets of CSI, and the result of preexisting genetic information. Where does
this information come from? Kauffman (1995) doesn't say, but the origin of such
information is an essential part of what needs to be explained in the history of
life. Similarly, in his light system, the order that allegedly arises for “for
free” actually arises only if the programmer of the model system “tunes” it in
such a way as to keep it from either (a) generating an excessively rigid order
or (b) developing into chaos (pp. 86-88). Yet this necessary tuning involves an
intelligent programmer selecting certain parameters and excluding others--that
is, inputting information.
Second, Kauffman's model systems are not
constrained by functional considerations and thus are not analogous to
biological systems. A system of interconnected lights governed by pre-programmed
rules may well settle into a small number of patterns within a much larger space
of possibilities. But because these patterns have no function, and need not meet
any functional requirements, they have no specificity analogous to that present
in actual organisms. Instead, examination of Kauffman's (1995) model systems
shows that they do not produce sequences or systems characterized by
specified complexity, but instead by large amounts of symmetrical order
or internal redundancy interspersed with aperiodicity or (mere) complexity (pp.
53, 89, 102). Getting a law-governed system to generate repetitive patterns of
flashing lights, even with a certain amount of variation, is clearly
interesting, but not biologically relevant. On the other hand, a system of
lights flashing the title of a Broadway play would model a biologically relevant
self-organizational process, at least if such a meaningful or functionally
specified sequence arose without intelligent agents previously programming the
system with equivalent amounts of CSI. In any case, Kauffman's systems do not
produce specified complexity, and thus do not offer promising models for
explaining the new genes and proteins that arose in the Cambrian.
so, Kauffman suggests that his self-organizational models can specifically
elucidate aspects of the Cambrian explosion. According to Kauffman
(1995:199-201), new Cambrian animals emerged as the result of “long jump”
mutations that established new body plans in a discrete rather than gradual
fashion. He also recognizes that mutations affecting early development are
almost inevitably harmful. Thus, he concludes that body plans, once established,
will not change, and that any subsequent evolution must occur within an
established body plan (Kauffman 1995:201). And indeed, the fossil record does
show a curious (from a neo-Darwinian point of view) top-down pattern of
appearance, in which higher taxa (and the body plans they represent) appear
first, only later to be followed by the multiplication of lower taxa
representing variations within those original body designs (Erwin et al. 1987,
Lewin 1988, Valentine & Jablonski 2003:518). Further, as Kauffman expects,
body plans appear suddenly and persist without significant modification over
But here, again, Kauffman begs the most important question, which
is: what produces the new Cambrian body plans in the first place? Granted, he
invokes “long jump mutations” to explain this, but he identifies no specific
self-organizational process that can produce such mutations. Moreover, he
concedes a principle that undermines the plausibility of his own proposal.
Kauffman acknowledges that mutations that occur early in development are almost
inevitably deleterious. Yet developmental biologists know that these are the
only kind of mutations that have a realistic chance of producing large-scale
evolutionary change--i.e., the big jumps that Kauffman invokes. Though Kauffman
repudiates the neo-Darwinian reliance upon random mutations in favor of
self-organizing order, in the end, he must invoke the most implausible kind of
random mutation in order to provide a self-organizational account of the new
Cambrian body plans. Clearly, his model is not sufficient.
Of course, still other causal explanations have been
proposed. During the 1970s, the paleontologists Eldredge and Gould (1972)
proposed the theory of evolution by punctuated equilibrium in order to account
for a pervasive pattern of “sudden appearance” and “stasis” in the fossil
record. Though advocates of punctuated equilibrium were mainly seeking to
describe the fossil record more accurately than earlier gradualist neo-Darwinian
models had done, they did also propose a mechanism--known as species
selection--by which the large morphological jumps evident in fossil record might
have been produced. According to punctuationalists, natural selection functions
more as a mechanism for selecting the fittest species rather than the most-fit
individual among a species. Accordingly, on this model, morphological change
should occur in larger, more discrete intervals than it would given a
traditional neo-Darwinian understanding.
Despite its virtues as a
descriptive model of the history of life, punctuated equilibrium has been widely
criticized for failing to provide a mechanism sufficient to produce the novel
form characteristic of higher taxonomic groups. For one thing, critics have
noted that the proposed mechanism of punctuated evolutionary change simply
lacked the raw material upon which to work. As Valentine and Erwin (1987) note,
the fossil record fails to document a large pool of species prior to the
Cambrian. Yet the proposed mechanism of species selection requires just such a
pool of species upon which to act. Thus, they conclude that the mechanism of
species selection probably does not resolve the problem of the origin of the
higher taxonomic groups (p. 96).8
Further, punctuated equilibrium has not addressed the more specific and
fundamental problem of explaining the origin of the new biological information
(whether genetic or epigenetic) necessary to produce novel biological form.
Advocates of punctuated equilibrium might assume that the new species (upon
which natural selection acts) arise by known microevolutionary processes of
speciation (such as founder effect, genetic drift or bottleneck effect) that do
not necessarily depend upon mutations to produce adaptive changes. But, in that
case, the theory lacks an account of how the specifically higher taxa
arise. Species selection will only produce more fit species. On the other hand,
if punctuationalists assume that processes of genetic mutation can produce more
fundamental morphological changes and variations, then their model becomes
subject to the same problems as neo-Darwinism (see above). This dilemma is
evident in Gould (2002:710) insofar as his attempts to explain adaptive
complexity inevitably employ classical neo-Darwinian modes of explanation.9
attempt to explain the origin of form has been proposed by the structuralists
such as Gerry Webster and Brian Goodwin (1984, 1996). These biologists, drawing
on the earlier work of D'Arcy Thompson (1942), view biological form as the
result of structural constraints imposed upon matter by morphogenetic rules or
laws. For reasons similar to those discussed above, the structuralists have
insisted that these generative or morphogenetic rules do not reside in the lower
level building materials of organisms, whether in genes or proteins. Webster and
Goodwin (1984:510-511) further envisioned morphogenetic rules or laws operating
ahistorically, similar to the way in which gravitational or electromagnetic laws
operate. For this reason, structuralists see phylogeny as of secondary
importance in understanding the origin of the higher taxa, though they think
that transformations of form can occur. For structuralists, constraints on the
arrangement of matter arise not mainly as the result of historical
contingencies--such as environmental changes or genetic mutations--but instead
because of the continuous ahistorical operation of fundamental laws of
form--laws that organize or inform matter.
While this approach avoids
many of the difficulties currently afflicting neo-Darwinism (in particular those
associated with its “genocentricity”), critics (such as Maynard Smith 1986) of
structuralism have argued that the structuralist explanation of form lacks
specificity. They note that structuralists have been unable to say just where
laws of form reside--whether in the universe, or in every possible world, or in
organisms as a whole, or in just some part of organisms. Further, according to
structuralists, morphogenetic laws are mathematical in character. Yet,
structuralists have yet to specify the mathematical formulae that determine
Others (Yockey 1992; Polanyi 1967, 1968; Meyer 2003)
have questioned whether physical laws could in principle generate the kind of
complexity that characterizes biological systems. Structuralists envision the
existence of biological laws that produce form in much the same way that
physical laws produce form. Yet the forms that physicists regard as
manifestations of underlying laws are characterized by large amounts of
symmetric or redundant order, by relatively simple patterns such as vortices or
gravitational fields or magnetic lines of force. Indeed, physical laws are
typically expressed as differential equations (or algorithms) that almost by
definition describe recurring phenomena--patterns of compressible “order” not
“complexity” as defined by algorithmic information theory (Yockey 1992:77-83).
Biological forms, by contrast, manifest greater complexity and derive in
ontogeny from highly complex initial conditions--i.e., non-redundant sequences
of nucleotide bases in the genome and other forms of information expressed in
the complex and irregular three-dimensional topography of the organism or the
fertilized egg. Thus, the kind of form that physical laws produce is not
analogous to biological form--at least not when compared from the standpoint of
(algorithmic) complexity. Further, physical laws lack the information content to
specify biology systems. As Polyanyi (1967, 1968) and Yockey (1992:290) have
shown, the laws of physics and chemistry allow, but do not determine,
distinctively biological modes of organization. In other words, living systems
are consistent with, but not deducible, from physical-chemical laws
Of course, biological systems do manifest some reoccurring
patterns, processes and behaviors. The same type of organism develops repeatedly
from similar ontogenetic processes in the same species. Similar processes of
cell division reoccur in many organisms. Thus, one might describe certain
biological processes as law-governed. Even so, the existence of such biological
regularities does not solve the problem of the origin of form and information,
since the recurring processes described by such biological laws (if there be
such laws) only occur as the result of preexisting stores of (genetic and/or
epigenetic) information and these information-rich initial conditions impose the
constraints that produce the recurring behavior in biological systems. (For
example, processes of cell division recur with great frequency in organisms, but
depend upon information-rich DNA and proteins molecules.) In other words,
distinctively biological regularities depend upon preexisting biological
information. Thus, appeals to higher-level biological laws presuppose, but do
not explain, the origination of the information necessary to
Thus, structuralism faces a difficult in principle
dilemma. On the one hand, physical laws produce very simple redundant patterns
that lack the complexity characteristic of biological systems. On the other
hand, distinctively biological laws--if there are such laws--depend upon
preexisting information-rich structures. In either case, laws are not good
candidates for explaining the origination of biological form or the information
necessary to produce it.
Cladism: An Artifact of
Some cladists have advanced another approach to the
problem of the origin of form, specifically as it arises in the Cambrian. They
have argued that the problem of the origin of the phyla is an artifact of the
classification system, and therefore, does not require explanation. Budd and
Jensen (2000), for example, argue that the problem of the Cambrian explosion
resolves itself if one keeps in mind the cladistic distinction between “stem”
and “crown” groups. Since crown groups arise whenever new characters are added
to simpler more ancestral stem groups during the evolutionary process, new phyla
will inevitably arise once a new stem group has arisen. Thus, for Budd and
Jensen what requires explanation is not the crown groups corresponding to the
new Cambrian phyla, but the earlier more primitive stem groups that presumably
arose deep in the Proterozoic. Yet since these earlier stem groups are by
definition less derived, explaining them will be considerably easier than
explaining the origin of the Cambrian animals de novo. In any case, for
Budd and Jensen the explosion of new phyla in the Cambrian does not require
explanation. As they put it, “given that the early branching points of major
clades is an inevitable result of clade diversification, the alleged phenomenon
of the phyla appearing early and remaining morphologically static is not seen to
require particular explanation” (Budd & Jensen 2000:253).
superficially plausible, perhaps, Budd and Jensen's attempt to explain away the
Cambrian explosion begs crucial questions. Granted, as new characters are added
to existing forms, novels morphology and greater morphological disparity will
likely result. But what causes new characters to arise? And how does the
information necessary to produce new characters originate? Budd and Jensen do
not specify. Nor can they say how derived the ancestral forms are likely to have
been, and what processes, might have been sufficient to produce them. Instead,
they simply assume the sufficiency of known neo-Darwinian mechanisms (Budd &
Jensen 2000:288). Yet, as shown above, this assumption is now problematic. In
any case, Budd and Jensen do not explain what causes the origination of
biological form and information.
Convergence and Teleological
More recently, Conway Morris (2000, 2003c) has suggested
another possible explanation based on the tendency for evolution to converge on
the same structural forms during the history of life. Conway Morris cites
numerous examples of organisms that possess very similar forms and structures,
even though such structures are often built from different material substrates
and arise (in ontogeny) by the expression of very different genes. Given the
extreme improbability of the same structures arising by random mutation and
selection in disparate phylogenies, Conway Morris argues that the pervasiveness
of convergent structures suggests that evolution may be in some way “channeled”
toward similar functional and/or structural endpoints. Such an end-directed
understanding of evolution, he admits, raises the controversial prospect of a
teleological or purposive element in the history of life. For this reason, he
argues that the phenomenon of convergence has received less attention than it
might have otherwise. Nevertheless, he argues that just as physicists have
reopened the question of design in their discussions of anthropic fine-tuning,
the ubiquity of convergent structures in the history of life has led some
biologists (Denton 1998) to consider extending teleological thinking to biology.
And, indeed, Conway Morris himself intimates that the evolutionary process might
be “underpinned by a purpose” (2000:8, 2003b:511).
Conway Morris, of
course, considers this possibility in relation to a very specific aspect of the
problem of organismal form, namely, the problem of explaining why the same forms
arise repeatedly in so many disparate lines of decent. But this raises a
question. Could a similar approach shed explanatory light on the more general
causal question that has been addressed in this review? Could the notion of
purposive design help provide a more adequate explanation for the origin of
organismal form generally? Are there reasons to consider design as an
explanation for the origin of the biological information necessary to produce
the higher taxa and their corresponding morphological novelty?
remainder of this review will suggest that there are such reasons. In so doing,
it may also help explain why the issue of teleology or design has reemerged
within the scientific discussion of biological origins (Denton 1986, 1998;
Thaxton et al. 1992; Kenyon & Mills 1996: Behe 1996, 2004; Dembski 1998,
2002, 2004; Conway Morris 2000, 2003a, 2003b, Lonnig 2001; Lonnig & Saedler
2002; Nelson & Wells 2003; Meyer 2003, 2004; Bradley 2004) and why some
scientists and philosophers of science have considered teleological explanations
for the origin of form and information despite strong methodological
prohibitions against design as a scientific hypothesis (Gillespie 1979, Lenior
First, the possibility of design as an explanation follows
logically from a consideration of the deficiencies of neo-Darwinism and other
current theories as explanations for some of the more striking “appearances of
design” in biological systems. Neo-Darwinists such as Ayala (1994:5), Dawkins
(1986:1), Mayr (1982:xi-xii) and Lewontin (1978) have long acknowledged that
organisms appear to have been designed. Of course, neo-Darwinists assert that
what Ayala (1994:5) calls the “obvious design” of living things is only apparent
since the selection/mutation mechanism can explain the origin of complex form
and organization in living systems without an appeal to a designing agent.
Indeed, neo-Darwinists affirm that mutation and selection--and perhaps other
similarly undirected mechanisms--are fully sufficient to explain the appearance
of design in biology. Self-organizational theorists and punctuationalists modify
this claim, but affirm its essential tenet. Self-organization theorists argue
that natural selection acting on self organizing order can explain the
complexity of living things--again, without any appeal to design.
Punctuationalists similarly envision natural selection acting on newly arising
species with no actual design involved.
And clearly, the neo-Darwinian
mechanism does explain many appearances of design, such as the adaptation of
organisms to specialized environments that attracted the interest of 19th
century biologists. More specifically, known microevolutionary processes appear
quite sufficient to account for changes in the size of Galapagos finch beaks
that have occurred in response to variations in annual rainfall and available
food supplies (Weiner 1994, Grant 1999).
But does neo-Darwinism, or any
other fully materialistic model, explain all appearances of design in biology,
including the body plans and information that characterize living systems?
Arguably, biological forms--such as the structure of a chambered nautilus, the
organization of a trilobite, the functional integration of parts in an eye or
molecular machine--attract our attention in part because the organized
complexity of such systems seems reminiscent of our own designs. Yet, this
review has argued that neo-Darwinism does not adequately account for the origin
of all appearances of design, especially if one considers animal body plans, and
the information necessary to construct them, as especially striking examples of
the appearance of design in living systems. Indeed, Dawkins (1995:11) and Gates
(1996:228) have noted that genetic information bears an uncanny resemblance to
computer software or machine code. For this reason, the presence of CSI in
living organisms, and the discontinuous increases of CSI that occurred during
events such as the Cambrian explosion, appears at least suggestive of
Does neo-Darwinism or any other purely materialistic model of
morphogenesis account for the origin of the genetic and other forms of CSI
necessary to produce novel organismal form? If not, as this review has argued,
could the emergence of novel information-rich genes, proteins, cell types and
body plans have resulted from actual design, rather than a purposeless process
that merely mimics the powers of a designing intelligence? The logic of
neo-Darwinism, with its specific claim to have accounted for the appearance of
design, would itself seem to open the door to this possibility. Indeed, the
historical formulation of Darwinism in dialectical opposition to the design
hypothesis (Gillespie 1979), coupled with the neo-Darwinism's inability to
account for many salient appearances of design including the emergence of form
and information, would seem logically to reopen the possibility of actual (as
opposed to apparent) design in the history of life.
A second reason for
considering design as an explanation for these phenomena follows from the
importance of explanatory power to scientific theory evaluation and from a
consideration of the potential explanatory power of the design hypothesis.
Studies in the methodology and philosophy of science have shown that many
scientific theories, particularly in the historical sciences, are formulated and
justified as inferences to the best explanation (Lipton 1991:32-88, Brush
1989:1124-1129, Sober 2000:44). Historical scientists, in particular, assess or
test competing hypotheses by evaluating which hypothesis would, if true, provide
the best explanation for some set of relevant data (Meyer 1991, 2002; Cleland
Those with greater explanatory power are typically judged to be better, more
probably true, theories. Darwin (1896:437) used this method of reasoning in
defending his theory of universal common descent. Moreover, contemporary studies
on the method of “inference to the best explanation” have shown that determining
which among a set of competing possible explanations constitutes the best
depends upon judgments about the causal adequacy, or “causal powers,” of
competing explanatory entities (Lipton 1991:32-88). In the historical sciences,
uniformitarian and/or actualistic (Gould 1965, Simpson 1970, Rutten 1971,
Hooykaas 1975) canons of method suggest that judgments about causal adequacy
should derive from our present knowledge of cause and effect relationships. For
historical scientists, “the present is the key to the past” means that present
experience-based knowledge of cause and effect relationships typically guides
the assessment of the plausibility of proposed causes of past events.
it is precisely for this reason that current advocates of the design hypothesis
want to reconsider design as an explanation for the origin of biological form
and information. This review, and much of the literature it has surveyed,
suggests that four of the most prominent models for explaining the origin of
biological form fail to provide adequate causal explanations for the
discontinuous increases of CSI that are required to produce novel morphologies.
Yet, we have repeated experience of rational and conscious agents--in particular
ourselves--generating or causing increases in complex specified information,
both in the form of sequence-specific lines of code and in the form of
hierarchically arranged systems of parts.
In the first place, intelligent
human agents--in virtue of their rationality and consciousness--have
demonstrated the power to produce information in the form of linear
sequence-specific arrangements of characters. Indeed, experience affirms that
information of this type routinely arises from the activity of intelligent
agents. A computer user who traces the information on a screen back to its
source invariably comes to a mind--that of a software engineer or
programmer. The information in a book or inscriptions ultimately derives from a
writer or scribe--from a mental, rather than a strictly material, cause. Our
experience-based knowledge of information-flow confirms that systems with large
amounts of specified complexity (especially codes and languages) invariably
originate from an intelligent source from a mind or personal agent. As Quastler
(1964) put it, the “creation of new information is habitually associated with
conscious activity” (p. 16). Experience teaches this obvious
Further, the highly specified hierarchical arrangements of parts
in animal body plans also suggest design, again because of our experience
of the kinds of features and systems that designers can and do produce. At every
level of the biological hierarchy, organisms require specified and highly
improbable arrangements of lower-level constituents in order to maintain their
form and function. Genes require specified arrangements of nucleotide bases;
proteins require specified arrangements of amino acids; new cell types require
specified arrangements of systems of proteins; body plans require specialized
arrangements of cell types and organs. Organisms not only contain
information-rich components (such as proteins and genes), but they comprise
information-rich arrangements of those components and the systems that comprise
them. Yet we know, based on our present experience of cause and effect
relationships, that design engineers--possessing purposive intelligence and
rationality--have the ability to produce information-rich hierarchies in which
both individual modules and the arrangements of those modules exhibit complexity
and specificity--information so defined. Individual transistors, resistors, and
capacitors exhibit considerable complexity and specificity of design; at a
higher level of organization, their specific arrangement within an integrated
circuit represents additional information and reflects further design. Conscious
and rational agents have, as part of their powers of purposive intelligence, the
capacity to design information-rich parts and to organize those parts into
functional information-rich systems and hierarchies. Further, we know of no
other causal entity or process that has this capacity. Clearly, we have good
reason to doubt that mutation and selection, self-organizational processes or
laws of nature, can produce the information-rich components, systems, and body
plans necessary to explain the origination of morphological novelty such as that
which arises in the Cambrian period.
There is a third reason to consider
purpose or design as an explanation for the origin of biological form and
information: purposive agents have just those necessary powers that natural
selection lacks as a condition of its causal adequacy. At several points in the
previous analysis, we saw that natural selection lacked the ability to generate
novel information precisely because it can only act after new functional
CSI has arisen. Natural selection can favor new proteins, and genes, but only
after they perform some function. The job of generating new functional genes,
proteins and systems of proteins therefore falls entirely to random mutations.
Yet without functional criteria to guide a search through the space of possible
sequences, random variation is probabilistically doomed. What is needed is not
just a source of variation (i.e., the freedom to search a space of
possibilities) or a mode of selection that can operate after the fact of a
successful search, but instead a means of selection that (a) operates during a
search--before success--and that (b) is guided by information about, or
knowledge of, a functional target.
Demonstration of this requirement has
come from an unlikely quarter: genetic algorithms. Genetic algorithms are
programs that allegedly simulate the creative power of mutation and selection.
Dawkins and Kuppers, for example, have developed computer programs that
putatively simulate the production of genetic information by mutation and
natural selection (Dawkins 1986:47-49, Kuppers 1987:355-369). Nevertheless, as
shown elsewhere (Meyer 1998:127-128, 2003:247-248), these programs only succeed
by the illicit expedient of providing the computer with a “target sequence” and
then treating relatively greater proximity to future function (i.e., the
target sequence), not actual present function, as a selection criterion. As
Berlinski (2000) has argued, genetic algorithms need something akin to a
“forward looking memory” in order to succeed. Yet such foresighted selection has
no analogue in nature. In biology, where differential survival depends upon
maintaining function, selection cannot occur before new functional sequences
arise. Natural selection lacks foresight.
What natural selection lacks,
intelligent selection--purposive or goal-directed design--provides. Rational
agents can arrange both matter and symbols with distant goals in mind. In using
language, the human mind routinely “finds” or generates highly improbable
linguistic sequences to convey an intended or preconceived idea. In the
process of thought, functional objectives precede and constrain the selection of
words, sounds and symbols to generate functional (and indeed meaningful)
sequences from among a vast ensemble of meaningless alternative combinations of
sound or symbol (Denton 1986:309-311). Similarly, the construction of complex
technological objects and products, such as bridges, circuit boards, engines and
software, result from the application of goal-directed constraints (Polanyi
1967, 1968). Indeed, in all functionally integrated complex systems where the
cause is known by experience or observation, design engineers or other
intelligent agents applied boundary constraints to limit possibilities in order
to produce improbable forms, sequences or structures. Rational agents have
repeatedly demonstrated the capacity to constrain the possible to actualize
improbable but initially unrealized future functions. Repeated experience
affirms that intelligent agents (minds) uniquely possess such causal
Analysis of the problem of the origin of biological information,
therefore, exposes a deficiency in the causal powers of natural selection that
corresponds precisely to powers that agents are uniquely known to possess.
Intelligent agents have foresight. Such agents can select functional goals
before they exist. They can devise or select material means to accomplish
those ends from among an array of possibilities and then actualize those goals
in accord with a preconceived design plan or set of functional requirements.
Rational agents can constrain combinatorial space with distant outcomes in mind.
The causal powers that natural selection lacks--almost by definition--are
associated with the attributes of consciousness and rationality--with purposive
intelligence. Thus, by invoking design to explain the origin of new biological
information, contemporary design theorists are not positing an arbitrary
explanatory element unmotivated by a consideration of the evidence. Instead,
they are positing an entity possessing precisely the attributes and causal
powers that the phenomenon in question requires as a condition of its production
An experience-based analysis of
the causal powers of various explanatory hypotheses suggests purposive or
intelligent design as a causally adequate--and perhaps the most causally
adequate--explanation for the origin of the complex specified information
required to build the Cambrian animals and the novel forms they represent. For
this reason, recent scientific interest in the design hypothesis is unlikely to
abate as biologists continue to wrestle with the problem of the origination of
biological form and the higher taxa.
Adams, M. D. Et alia. 2000. The genome sequence of
Drosophila melanogaster.--Science 287:2185-2195.
& Z. Yang. 2003. Bayesian models of episodic evolution support a late
Precambrian explosive diversification of the Metazoa.--Molecular Biology and
Arthur, W. 1997. The origin of animal body plans.
Cambridge University Press, Cambridge, United Kingdom.
Axe, D. D. 2000.
Extreme functional sensitivity to conservative amino acid changes on enzyme
exteriors.--Journal of Molecular Biology 301(3):585-596.
Estimating the prevalence of protein sequences adopting functional enzyme
folds.--Journal of Molecular Biology (in press).
Ayala, F. 1994. Darwin's
revolution. Pp. 1-17 in J. Campbell and J. Schopf, eds., Creative
evolution?! Jones and Bartlett Publishers, Boston, Massachusetts.
______. A. Rzhetsky, & F. J. Ayala. 1998. Origin of the metazoan
phyla: molecular clocks confirm paleontological estimates--Proceedings of the
National Academy of Sciences USA. 95:606-611.
Becker, H., & W.
Lonnig, 2001. Transposons: eukaryotic. Pp. 529-539 in Nature encyclopedia
of life sciences, vol. 18. Nature Publishing Group, London, United
Behe, M. 1992. Experimental support for regarding functional
classes of proteins to be highly isolated from each other. Pp. 60-71 in
J. Buell and V. Hearn, eds., Darwinism: science or philosophy? Foundation for
Thought and Ethics, Richardson, Texas.
______. 1996. Darwin's black box.
The Free Press, New York.
______. 2004. Irreducible complexity: obstacle
to Darwinian evolution. Pp. 352-370 in W. A. Dembski and M. Ruse, eds.,
Debating design: from Darwin to DNA. Cambridge University Press, Cambridge,
Benton, M., & F. J. Ayala. 2003. Dating the tree of
Berlinski, D. 2000. “On assessing genetic
algorithms.” Public lecture. Conference: Science and evidence of design in the
universe. Yale University, November 4, 2000.
Blanco, F., I. Angrand,
& L. Serrano. 1999. Exploring the confirmational properties of the sequence
space between two proteins with different folds: an experimental study.--Journal
of Molecular Biology 285:741-753.
Bowie, J., & R. Sauer. 1989.
Identifying determinants of folding and activity for a protein of unknown
sequences: tolerance to amino acid substitution.--Proceedings of the National
Academy of Sciences, U.S.A. 86:2152-2156.
Bowring, S. A., J. P.
Grotzinger, C. E. Isachsen, A. H. Knoll, S. M. Pelechaty, & P. Kolosov.
1993. Calibrating rates of early Cambrian evolution.--Science
______. 1998a. A new look at evolutionary rates in deep
time: Uniting paleontology and high-precision geochronology.--GSA Today
______. 1998b. Geochronology comes of age.--Geotimes
Bradley, W. 2004. Information, entropy and the origin of life.
Pp. 331-351 in W. A. Dembski and M. Ruse, eds., Debating design: from
Darwin to DNA. Cambridge University Press, Cambridge, United
Brocks, J. J., G. A. Logan, R. Buick, & R. E. Summons. 1999.
Archean molecular fossils and the early rise of eukaryotes.--Science
Brush, S. G. 1989. Prediction and theory evaluation: the
case of light bending.--Science 246:1124-1129.
Budd, G. E. & S. E.
Jensen. 2000. A critical reappraisal of the fossil record of the bilaterial
phyla.--Biological Reviews of the Cambridge Philosophical Society
Carroll, R. L. 2000. Towards a new evolutionary
synthesis.--Trends in Ecology and Evolution 15:27-32.
Cleland, C. 2001.
Historical science, experimental science, and the scientific method.--Geology
______. 2002. Methodological and epistemic differences
between historical science and experimental science.--Philosophy of Science
Chothia, C., I. Gelfland, & A. Kister. 1998. Structural
determinants in the sequences of immunoglobulin variable domain.--Journal of
Molecular Biology 278:457-479.
Conway Morris, S. 1998a. The question of
metazoan monophyly and the fossil record.--Progress in Molecular and Subcellular
______. 1998b. Early Metazoan evolution: Reconciling
paleontology and molecular biology.--American Zoologist 38
______. 2000. Evolution: bringing molecules into the
______. 2003a. The Cambrian “explosion” of
metazoans. Pp. 13-32 in G. B. Muller and S. A. Newman, eds., Origination
of organismal form: beyond the gene in developmental and evolutionary biology.
The M.I.T. Press, Cambridge, Massachusetts.
______. 2003b. Cambrian
“explosion” of metazoans and molecular biology: would Darwin be
satisfied?--International Journal of Developmental Biology
______. 2003c. Life's solution: inevitable humans in a
lonely universe. Cambridge University Press, Cambridge, United
Crick, F. 1958. On protein synthesis.--Symposium for the Society
of Experimental Biology. 12(1958):138-163.
Darwin, C. 1859. On the origin
of species. John Murray, London, United Kingdom.
______. 1896. Letter to
Asa Gray. P. 437 in F. Darwin, ed., Life and letters of Charles Darwin,
vol. 1., D. Appleton, London, United Kingdom.
Davidson, E. 2001. Genomic
regulatory systems: development and evolution. Academic Press, New York, New
Dawkins, R. 1986. The blind watchmaker. Penguin Books, London,
______. 1995. River out of Eden. Basic Books, New
______. 1996. Climbing Mount Improbable. W. W. Norton &
Company, New York.
Dembski, W. A. 1998. The design inference. Cambridge
University Press, Cambridge, United Kingdom.
______. 2002. No free lunch:
why specified complexity cannot be purchased without intelligence. Rowman &
Littlefield, Lanham, Maryland.
______. 2004. The logical underpinnings of
intelligent design. Pp. 311-330 in W. A. Dembski and M. Ruse, eds.,
Debating design: from Darwin to DNA. Cambridge University Press, Cambridge,
Denton, M. 1986. Evolution: a theory in crisis. Adler
& Adler, London, United Kingdom.
______. 1998. Nature's density. The
Free Press, New York.
Eden, M. 1967. The inadequacies of neo-Darwinian
evolution as a scientific theory. Pp. 5-12 in P. S. Morehead and M. M.
Kaplan, eds., Mathematical challenges to the Darwinian interpretation of
evolution. Wistar Institute Symposium Monograph, Allen R. Liss, New
Eldredge, N., & S. J. Gould. 1972. Punctuated equilibria: an
alternative to phyletic gradualism. Pp. 82-115 in T. Schopf, ed., Models
in paleobiology. W. H. Freeman, San Francisco.
Erwin, D. H. 1994. Early
introduction of major morphological innovations.--Acta Palaeontologica Polonica
______. 2000. Macroevolution is more than repeated rounds of
microevolution.--Evolution & Development 2:78-84.
______. 2004. One
very long argument.--Biology and Philosophy 19:17-28.
Valentine, & D. Jablonski. 1997. The origin of animal body plans.--American
______, ______, & J. J. Sepkoski. 1987. A
comparative study of diversification events: the early Paleozoic versus the
Foote, M. 1997. Sampling, taxonomic
description, and our evolving knowledge of morphological
______, J. P. Hunter, C. M. Janis,
& J. J. Sepkoski. 1999. Evolutionary and preservational constraints on
origins of biologic groups: Divergence times of eutherian mammals.--Science
Frankel, J. 1980. Propagation of cortical differences in
Gates, B. 1996. The road ahead.
Blue Penguin, Boulder, Colorado.
Gerhart, J., & M. Kirschner. 1997.
Cells, embryos, and evolution. Blackwell Science, London, United
Gibbs, W. W. 2003. The unseen genome: gems among the
junk.--Scientific American. 289:46-53.
Gilbert, S. F., J. M. Opitz, &
R. A. Raff. 1996. Resynthesizing evolutionary and developmental
biology.--Developmental Biology 173:357-372.
Gillespie, N. C. 1979.
Charles Darwin and the problem of creation. University of Chicago Press,
Goodwin, B. C. 1985. What are the causes of
______. 1995. How the leopard changed
its spots: the evolution of complexity. Scribner's, New York, New
Gould, S. J. 1965. Is uniformitarianism necessary?--American
Journal of Science 263:223-228.
Gould, S. J. 2002. The structure of
evolutionary theory. Harvard University Press, Cambridge, Massachusetts.
Grant, P. R. 1999. Ecology and evolution of Darwin's finches. Princeton
University Press, Princeton, New Jersey.
Grimes, G. W., & K. J.
Aufderheide. 1991. Cellular aspects of pattern formation: the problem of
assembly. Monographs in Developmental Biology, vol. 22. Karger, Baseline,
Grotzinger, J. P., S. A. Bowring, B. Z. Saylor, & A. J.
Kaufman. 1995. Biostratigraphic and geochronologic constraints on early animal
Harold, F. M. 1995. From morphogenes to
______. 2001. The way of the
cell: molecules, organisms, and the order of life. Oxford University Press, New
Hodge, M. J. S. 1977. The structure and strategy of Darwin's long
argument.--British Journal for the History of Science
Hooykaas, R. 1975. Catastrophism in geology, its scientific
character in relation to actualism and uniformitarianism. Pp. 270-316 in
C. Albritton, ed., Philosophy of geohistory (1785-1970). Dowden, Hutchinson
& Ross, Stroudsburg, Pennsylvania.
John, B., & G. Miklos. 1988.
The eukaryote genome in development and evolution. Allen & Unwinding,
London, United Kingdom.
Kauffman, S. 1995. At home in the universe.
Oxford University Press, Oxford, United Kingdom.
Kenyon, D., & G.
Mills. 1996. The RNA world: a critique.--Origins & Design
Kerr, R. A. 1993. Evolution's Big Bang gets even more
explosive.-- Science 261:1274-1275.
Kimura, M. 1983. The neutral theory
of molecular evolution. Cambridge University Press, Cambridge, United
Koonin, E. 2000. How many genes can make a cell?: the minimal
genome concept.--Annual Review of Genomics and Human Genetics
Kuppers, B. O. 1987. On the prior probability of the existence
of life. Pp. 355-369 in L. Kruger et al., eds., The probabilistic
revolution. M.I.T. Press, Cambridge, Massachusetts.
Lange, B. M. H., A.
J. Faragher, P. March, & K. Gull. 2000. Centriole duplication and maturation
in animal cells. Pp. 235-249 in R. E. Palazzo and G. P. Schatten, eds.,
The centrosome in cell replication and early development. Current Topics in
Developmental Biology, vol. 49. Academic Press, San Diego.
A., & G. Struhl. 1996. Morphogens, compartments and pattern: lessons from
Lenior, T. 1982. The strategy of life.
University of Chicago Press, Chicago.
Levinton, J. 1988. Genetics,
paleontology, and macroevolution. Cambridge University Press, Cambridge, United
______. 1992. The big bang of animal evolution.--Scientific
Lewin, R. 1988. A lopsided look at
Lewontin, R. 1978. Adaptation. Pp. 113-125
in Evolution: a Scientific American book. W. H. Freeman & Company,
Lipton, P. 1991. Inference to the best explanation.
Routledge, New York.
Lonnig, W. E. 2001. Natural selection. Pp. 1008-1016
in W. E. Craighead and C. B. Nemeroff, eds., The Corsini encyclopedia of
psychology and behavioral sciences, 3rd edition, vol. 3. John Wiley & Sons,
______, & H. Saedler. 2002. Chromosome rearrangements and
transposable elements.--Annual Review of Genetics 36:389-410.
1979. Semantics, logic and vulgate neo-darwinism.--Evolutionary Theory
Marshall, W. F. & J. L. Rosenbaum. 2000. Are there nucleic
acids in the centrosome? Pp. 187-205 in R. E. Palazzo and G. P. Schatten,
eds., The centrosome in cell replication and early development. Current Topics
in Developmental Biology, vol. 49. San Diego, Academic Press.
Smith, J. 1986. Structuralism versus selection--is Darwinism enough? Pp. 39-46
in S. Rose and L. Appignanesi, eds., Science and Beyond. Basil Blackwell,
London, United Kingdom.
Mayr, E. 1982. Foreword. Pp. xi-xii in M.
Ruse, Darwinism defended. Pearson Addison Wesley, Boston, Massachusetts.
McDonald, J. F. 1983. The molecular basis of adaptation: a critical
review of relevant ideas and observations.--Annual Review of Ecology and
McNiven, M. A. & K. R. Porter. 1992. The
centrosome: contributions to cell form. Pp. 313-329 in V. I. Kalnins,
ed., The centrosome. Academic Press, San Diego.
Meyer, S. C. 1991. Of
clues and causes: a methodological interpretation of origin of life studies.
Unpublished doctoral dissertation, University of Cambridge, Cambridge, United
______. 1998. DNA by design: an inference to the best
explanation for the origin of biological information.--Rhetoric & Public
______. The scientific status of intelligent
design: The methodological equivalence of naturalistic and non-naturalistic
origins theories. Pp. 151-211 in Science and evidence for design in the
universe. Proceedings of the Wethersfield Institute. Ignatius Press, San
______. 2003. DNA and the origin of life: information,
specification and explanation. Pp. 223-285 in J. A. Campbell and S. C.
Meyer, eds., Darwinism, design and public education. Michigan State University
Press, Lansing, Michigan.
______. 2004. The Cambrian information
explosion: evidence for intelligent design. Pp. 371-391 in W. A. Dembski
and M. Ruse, eds., Debating design: from Darwin to DNA. Cambridge University
Press, Cambridge, United Kingdom.
______, M. Ross, P. Nelson, & P.
Chien. 2003. The Cambrian explosion: biology's big bang. Pp. 323-402 in
J. A. Campbell & S. C. Meyer, eds., Darwinism, design and public education.
Michigan State University Press, Lansing. See also Appendix C: Stratigraphic
first appearance of phyla body plans, pp. 593-598.
Miklos, G. L. G. 1993.
Emergence of organizational complexities during metazoan evolution: perspectives
from molecular biology, palaeontology and neo-Darwinism.--Mem. Ass. Australas.
Monastersky, R. 1993. Siberian rocks clock
biological big bang.--Science News 144:148.
Moss, L. 2004. What genes
can't do. The M.I.T. Press, Cambridge, Massachusetts.
Muller, G. B.
& S. A. Newman. 2003. Origination of organismal form: the forgotten cause in
evolutionary theory. Pp. 3-12 in G. B. Muller and S. A. Newman, eds.,
Origination of organismal form: beyond the gene in developmental and
evolutionary biology. The M.I.T. Press, Cambridge, Massachusetts.
Nanney, D. L. 1983. The ciliates and the cytoplasm.--Journal of
Nelson, P., & J. Wells. 2003. Homology in
biology: problem for naturalistic science and prospect for intelligent design.
Pp. 303-322 in J. A. Campbell and S. C. Meyer, eds., Darwinism, design
and public education. Michigan State University Press, Lansing.
H. F. 1990. Metaphors and the role of genes in development.--BioEssays
Nusslein-Volhard, C., & E. Wieschaus. 1980. Mutations
affecting segment number and polarity in Drosophila.--Nature
Ohno, S. 1996. The notion of the Cambrian pananimalia
genome.--Proceedings of the National Academy of Sciences, U.S.A.
Orgel, L. E., & F. H. Crick. 1980. Selfish DNA: the
ultimate parasite.--Nature 284:604-607.
Perutz, M. F., & H. Lehmann.
1968. Molecular pathology of human hemoglobin.--Nature
Polanyi, M. 1967. Life transcending physics and
chemistry.--Chemical and Engineering News, 45(35):54-66.
Life's irreducible structure.--Science 160:1308-1312, especially p.
Pourquie, O. 2003. Vertebrate somitogenesis: a novel paradigm for
animal segmentation?--International Journal of Developmental Biology
Quastler, H. 1964. The emergence of biological
organization. Yale University Press, New Haven, Connecticut.
1999. Larval homologies and radical evolutionary changes in early development,
Pp. 110-121 in Homology. Novartis Symposium, vol. 222. John Wiley &
Sons, Chichester, United Kingdom.
Reidhaar-Olson, J., & R. Sauer.
1990. Functionally acceptable solutions in two alpha-helical regions of lambda
repressor.--Proteins, Structure, Function, and Genetics,
Rutten, M. G. 1971. The origin of life by natural causes.
Sapp, J. 1987. Beyond the gene. Oxford University
Press, New York.
Sarkar, S. 1996. Biological information: a skeptical
look at some central dogmas of molecular biology. Pp. 187-233 in S.
Sarkar, ed., The philosophy and history of molecular biology: new perspectives.
Kluwer Academic Publishers, Dordrecht.
Schutzenberger, M. 1967.
Algorithms and the neo-Darwinian theory of evolution. Pp. 73-75 in P. S.
Morehead and M. M. Kaplan, eds., Mathematical challenges to the Darwinian
interpretation of evolution. Wistar Institute Symposium Monograph. Allen R.
Liss, New York.
Shannon, C. 1948. A mathematical theory of
communication.--Bell System Technical Journal 27:379-423, 623-656.
D. G., H. L. Loud, S. Conway Morris, X. L. Zhang, S. X. Hu, L. Chen, J. Han, M.
Zhu, Y. Li, & L. Z. Chen. 1999. Lower Cambrian vertebrates from south
Shubin, N. H., & C. R. Marshall. 2000.
Fossils, genes, and the origin of novelty. Pp. 324-340 in Deep time. The
Simpson, G. 1970. Uniformitarianism: an inquiry
into principle, theory, and method in geohistory and biohistory. Pp. 43-96 in M.
K. Hecht and W. C. Steered, eds., Essays in evolution and genetics in honor of
Theodosius Dobzhansky. Appleton-Century-Crofts, New York.
Sober, E. 2000.
The philosophy of biology, 2nd edition. Westview Press, San
Sonneborn, T. M. 1970. Determination, development, and
inheritance of the structure of the cell cortex. In Symposia of the
International Society for Cell Biology 9:1-13.
Sole, R. V., P. Fernandez,
& S. A. Kauffman. 2003. Adaptive walks in a gene network model of
morphogenesis: insight into the Cambrian explosion.--International Journal of
Developmental Biology 47(7-8):685-693.
Stadler, B. M. R., P. F. Stadler,
G. P. Wagner, & W. Fontana. 2001. The topology of the possible: formal
spaces underlying patterns of evolutionary change.--Journal of Theoretical
Steiner, M., & R. Reitner. 2001. Evidence of
organic structures in Ediacara-type fossils and associated microbial
Taylor, S. V., K. U. Walter, P. Kast,
& D. Hilvert. 2001. Searching sequence space for protein
catalysts.--Proceedings of the National Academy of Sciences, U.S.A.
Thaxton, C. B., W. L. Bradley, & R. L. Olsen. 1992.
The mystery of life's origin: reassessing current theories. Lewis and Stanley,
Thompson, D. W. 1942. On growth and form, 2nd edition.
Cambridge University Press, Cambridge, United Kingdom.
Thomson, K. S.
1992. Macroevolution: The morphological problem.--American Zoologist
Valentine, J. W. 1995. Late Precambrian bilaterians: grades
and clades. Pp. 87-107 in W. M. Fitch and F. J. Ayala, eds., Temporal and
mode in evolution: genetics and paleontology 50 years after Simpson. National
Academy Press, Washington, D.C.
______. 2004. On the origin of phyla.
University of Chicago Press, Chicago, Illinois.
______, & D. H.
Erwin, 1987. Interpreting great developmental experiments: the fossil record.
Pp. 71-107 in R. A. Raff and E. C. Raff, eds., Development as an
evolutionary process. Alan R. Liss, New York.
______, & D. Jablonski.
2003. Morphological and developmental macroevolution: a paleontological
perspective.--International Journal of Developmental Biology
Wagner, G. P. 2001. What is the promise of developmental
evolution? Part II: A causal explanation of evolutionary innovations may be
impossible.--Journal of Experimental Zoology (Mol. Dev. Evol.)
______, & P. F. Stadler. 2003. Quasi-independence,
homology and the Unity-C of type: a topological theory of characters.--Journal
of Theoretical Biology 220:505-527.
Webster, G., & B. Goodwin. 1984.
A structuralist approach to morphology.--Rivista di Biologia
______, & ______. 1996. Form and transformation:
generative and relational principles in biology. Cambridge University Press,
Cambridge, United Kingdom.
Weiner, J. 1994. The beak of the finch.
Vintage Books, New York.
Willmer, P. 1990. Invertebrate relationships:
patterns in animal evolution. Cambridge University Press, Cambridge, United
______. 2003. Convergence and homoplasy in the evolution of
organismal form. Pp. 33-50 in G. B. Muller and S. A. Newman, eds.,
Origination of organismal form: beyond the gene in developmental and
evolutionary biology. The M.I.T. Press, Cambridge, Massachusetts.
C. 1998. The universal ancestor.--Proceedings of the National Academy of
Sciences, U.S.A. 95:6854-6859.
Wray, G. A., J. S. Levinton, & L. H.
Shapiro. 1996. Molecular evidence for deep Precambrian divergences among
metazoan phyla.--Science 274:568-573.
Yockey, H. P. 1978. A calculation
of the probability of spontaneous biogenesis by information theory.--Journal of
Theoretical Biology 67:377-398.
______, 1992. Information theory and
molecular biology, Cambridge University Press, Cambridge, United
Specifically, Gilbert et al. (1996) argued that changes in morphogenetic fields
might produce large-scale changes in the developmental programs and, ultimately,
body plans of organisms. Yet they offered no evidence that such fields--if
indeed they exist--can be altered to produce advantageous variations in body
plan, though this is a necessary condition of any successful causal theory of
2 If one takes the fossil
record at face value and assumes that the Cambrian explosion took place within a
relatively narrow 5-10 million year window, explaining the origin of the
information necessary to produce new proteins, for example, becomes more acute
in part because mutation rates would not have been sufficient to generate the
number of changes in the genome necessary to build the new proteins for more
complex Cambrian animals (Ohno 1996:8475-8478). This review will argue that,
even if one allows several hundred million years for the origin of the metazoan,
significant probabilistic and other difficulties remain with the neo-Darwinian
explanation of the origin of form and information.
3 As Crick put it, “information means here the
precise determination of sequence, either of bases in the nucleic acid or
on amino acid residues in the protein” (Crick 1958:144, 153).
4 To solve this problem Ohno himself proposes the existence
of a hypothetical ancestral form that possessed virtually all the genetic
information necessary to produce the new body plans of the Cambrian animals. He
asserts that this ancestor and its “pananimalian genome” might have arisen
several hundred million years before the Cambrian explosion. On this view, each
of the different Cambrian animals would have possessed virtually identical
genomes, albeit with considerable latent and unexpressed capacity in the case of
each individual form (Ohno 1996:8475-8478). While this proposal might help
explain the origin of the Cambrian animal forms by reference to preexisting
genetic information, it does not solve, but instead merely displaces, the
problem of the origin of the genetic information necessary to produce these new
5 Some have suggested that mutations
in “master regulator” Hox genes might provide the raw material for body plan
morphogenesis. Yet there are two problems with this proposal. First, Hox gene
expression begins only after the foundation of the body plan has been
established in early embryogenesis. (Davidson 2001:66). Second, Hox genes are
highly conserved across many disparate phyla and so cannot account for the
morphological differences that exist between the phyla (Valentine
6 Notable differences in the
developmental pathways of similar organisms have been observed. For example,
congeneric species of sea urchins (from genus Heliocidaris) exhibit
striking differences in their developmental pathways (Raff 1999:110-121). Thus,
it might be argued that such differences show that early developmental programs
can in fact be mutated to produce new forms. Nevertheless, there are two
problems with this claim. First, there is no direct evidence that existing
differences in sea urchin development arose by mutation. Second, the observed
differences in the developmental programs of different species of sea urchins do
not result in new body plans, but instead in highly conserved structures.
Despite differences in developmental patterns, the endpoints are the same. Thus,
even if it can be assumed that mutations produced the differences in
developmental pathways, it must be acknowledged that such changes did not result
in novel form.
7 Of course, many
post-translation processes of modification also play a role in producing a
functional protein. Such processes make it impossible to predict a protein's
final sequencing from its corresponding gene sequence alone (Sarkar
8 Erwin (2004:21), although
friendly to the possibility of species selection, argues that Gould provides
little evidence for its existence. “The difficulty” writes Erwin of species
selection, “...is that we must rely on Gould's arguments for theoretical
plausibility and sufficient relative frequency. Rarely is a mass of data
presented to justify and support Gould's conclusion.” Indeed, Gould (2002)
himself admitted that species selection remains largely a hypothetical
construct: “I freely admit that well-documented cases of species selection do
not permeate the literature” (p. 710).
do not deny either the wonder, or the powerful importance, of organized adaptive
complexity. I recognize that we know no mechanism for the origin of such
organismal features other than conventional natural selection at the organismic
level--for the sheer intricacy and elaboration of good biomechanical design
surely precludes either random production, or incidental origin as a side
consequence of active processes at other levels” (Gould 2002:710). “Thus, we do
not challenge the efficacy or the cardinal importance of organismal selection.
As previously discussed, I fully agree with Dawkins (1986) and others that one
cannot invoke a higher-level force like species selection to explain 'things
that organisms do'--in particular, the stunning panoply of organismic
adaptations that has always motivated our sense of wonder about the natural
world, and that Darwin (1859) described, in one of his most famous lines (3), as
'that perfection of structure and coadaptation which most justly excites our
admiration'“ (Gould 2002:886).
in the historical sciences typically make claims about what happened in the
past, or what happened in the past to cause particular events to occur (Meyer
1991:57-72). For this reason, historical scientific theories are rarely tested
by making predictions about what will occur under controlled laboratory
conditions (Cleland 2001:987, 2002:474-496). Instead, such theories are usually
tested by comparing their explanatory power against that of their competitors
with respect to already known facts. Even in the case in which historical
theories make claims about past causes they usually do so on the basis of
preexisting knowledge of cause and effect relationships. Nevertheless,
prediction may play a limited role in testing historical scientific theories
since such theories may have implications as to what kind of evidence is likely
to emerge in the future. For example, neo-Darwinism affirms that new functional
sections of the genome arise by trial and error process of mutation and
subsequent selection. For this reason, historically many neo-Darwinists expected
or predicted that the large non-coding regions of the genome--so-called “junk
DNA”--would lack function altogether (Orgel & Crick 1980). On this line of
thinking, the nonfunctional sections of the genome represent nature's failed
experiments that remain in the genome as a kind of artifact of the past activity
of the mutation and selection process. Advocates of the design hypotheses on the
other hand, would have predicted that non-coding regions of the genome might
well reveal hidden functions, not only because design theorists do not think
that new genetic information arises by a trial and error process of mutation and
selection, but also because designed systems are often functionally polyvalent.
Even so, as new studies reveal more about the functions performed by the
non-coding regions of the genome (Gibbs 2003), the design hypothesis can no
longer be said to make this claim in the form of a specifically future-oriented
prediction. Instead, the design hypothesis might be said to gain confirmation or
support from its ability to explain this now known evidence, albeit after the
fact. Of course, neo Darwinists might also amend their original prediction using
various auxiliary hypotheses to explain away the presence of newly discovered
functions in the non-coding regions of DNA. In both cases, considerations of
ex post facto explanatory power reemerge as central to assessing and
testing competing historical theories.