Re: OT: let's ignore bvallely's political postings
- From: "bvallely@xxxxxxx" <bvallely@xxxxxxx>
- Date: Mon, 9 Feb 2009 15:24:32 -0800 (PST)
...
..No, both are science.
Show me the data. Show me the experiments. Show me the research.
ntelligent Design: The Origin of Biological Information and the Higher
Taxonomic Categories
By: Stephen C. Meyer
Proceedings of the Biological Society of Washington
May 18, 2007
On August 4th, 2004 an extensive review essay by Dr. Stephen C. Meyer,
Director of Discovery Institute's Center for Science & Culture
appeared in the Proceedings of the Biological Society of Washington
(volume 117, no. 2, pp. 213-239). The Proceedings is a peer-reviewed
biology journal published at the National Museum of Natural History at
the Smithsonian Institution in Washington D.C.
In the article, entitled “The Origin of Biological Information and the
Higher Taxonomic Categories”, Dr. Meyer argues that no current
materialistic theory of evolution can account for the origin of the
information necessary to build novel animal forms. He proposes
intelligent design as an alternative explanation for the origin of
biological information and the higher taxa.
Due to an unusual number of inquiries about the article, Dr. Meyer,
the copyright holder, has decided to make the article available now in
HTML format on this website. (Off prints are also available from
Discovery Institute by writing to Rob Crowther at:
cscinfo@xxxxxxxxxxxxxx Please provide your mailing address and we will
dispatch a copy).
En Espa�ol (PDF)
PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON
117(2):213-239. 2004
The origin of biological information and the higher taxonomic
categories
Stephen C. Meyer
Introduction
In a recent volume of the Vienna Series in a Theoretical Biology
(2003), Gerd B. Muller and Stuart Newman argue that what they call the
“origination of organismal form” remains an unsolved problem. In
making this claim, Muller and Newman (2003:3-10) distinguish two
distinct issues, namely, (1) the causes of form generation in the
individual organism during embryological development and (2) the
causes responsible for the production of novel organismal forms in the
first place during the history of life. To distinguish the latter case
(phylogeny) from the former (ontogeny), Muller and Newman use the term
“origination” to designate the causal processes by which biological
form first arose during the evolution of life. They insist that “the
molecular mechanisms that bring about biological form in modern day
embryos should not be confused” with the causes responsible for the
origin (or “origination”) of novel biological forms during the history
of life (p.3). They further argue that we know more about the causes
of ontogenesis, due to advances in molecular biology, molecular
genetics and developmental biology, than we do about the causes of
phylogenesis--the ultimate origination of new biological forms during
the remote past.
In making this claim, Muller and Newman are careful to affirm that
evolutionary biology has succeeded in explaining how preexisting forms
diversify under the twin influences of natural selection and variation
of genetic traits. Sophisticated mathematically-based models of
population genetics have proven adequate for mapping and understanding
quantitative variability and populational changes in organisms. Yet
Muller and Newman insist that population genetics, and thus
evolutionary biology, has not identified a specifically causal
explanation for the origin of true morphological novelty during the
history of life. Central to their concern is what they see as the
inadequacy of the variation of genetic traits as a source of new form
and structure. They note, following Darwin himself, that the sources
of new form and structure must precede the action of natural selection
(2003:3)--that selection must act on what already exists. Yet, in
their view, the “genocentricity” and “incrementalism” of the neo-
Darwinian mechanism has meant that an adequate source of new form and
structure has yet to be identified by theoretical biologists. Instead,
Muller and Newman see the need to identify epigenetic sources of
morphological innovation during the evolution of life. In the
meantime, however, they insist neo-Darwinism lacks any “theory of the
generative” (p. 7).
As it happens, Muller and Newman are not alone in this judgment. In
the last decade or so a host of scientific essays and books have
questioned the efficacy of selection and mutation as a mechanism for
generating morphological novelty, as even a brief literature survey
will establish. Thomson (1992:107) expressed doubt that large-scale
morphological changes could accumulate via minor phenotypic changes at
the population genetic level. Miklos (1993:29) argued that neo-
Darwinism fails to provide a mechanism that can produce large-scale
innovations in form and complexity. Gilbert et al. (1996) attempted to
develop a new theory of evolutionary mechanisms to supplement
classical neo-Darwinism, which, they argued, could not adequately
explain macroevolution. As they put it in a memorable summary of the
situation: “starting in the 1970s, many biologists began questioning
its (neo-Darwinism's) adequacy in explaining evolution. Genetics might
be adequate for explaining microevolution, but microevolutionary
changes in gene frequency were not seen as able to turn a reptile into
a mammal or to convert a fish into an amphibian. Microevolution looks
at adaptations that concern the survival of the fittest, not the
arrival of the fittest. As Goodwin (1995) points out, 'the origin of
species--Darwin's problem--remains unsolved'“ (p. 361). Though Gilbert
et al. (1996) attempted to solve the problem of the origin of form by
proposing a greater role for developmental genetics within an
otherwise neo-Darwinian framework,1 numerous recent authors have
continued to raise questions about the adequacy of that framework
itself or about the problem of the origination of form generally
(Webster & Goodwin 1996; Shubin & Marshall 2000; Erwin 2000; Conway
Morris 2000, 2003b; Carroll 2000; Wagner 2001; Becker & Lonnig 2001;
Stadler et al. 2001; Lonnig & Saedler 2002; Wagner & Stadler 2003;
Valentine 2004:189-194).
What lies behind this skepticism? Is it warranted? Is a new and
specifically causal theory needed to explain the origination of
biological form?
This review will address these questions. It will do so by analyzing
the problem of the origination of organismal form (and the
corresponding emergence of higher taxa) from a particular theoretical
standpoint. Specifically, it will treat the problem of the origination
of the higher taxonomic groups as a manifestation of a deeper problem,
namely, the problem of the origin of the information (whether genetic
or epigenetic) that, as it will be argued, is necessary to generate
morphological novelty.
In order to perform this analysis, and to make it relevant and
tractable to systematists and paleontologists, this paper will examine
a paradigmatic example of the origin of biological form and
information during the history of life: the Cambrian explosion. During
the Cambrian, many novel animal forms and body plans (representing new
phyla, subphyla and classes) arose in a geologically brief period of
time. The following information-based analysis of the Cambrian
explosion will support the claim of recent authors such as Muller and
Newman that the mechanism of selection and genetic mutation does not
constitute an adequate causal explanation of the origination of
biological form in the higher taxonomic groups. It will also suggest
the need to explore other possible causal factors for the origin of
form and information during the evolution of life and will examine
some other possibilities that have been proposed.
The Cambrian Explosion
The “Cambrian explosion” refers to the geologically sudden appearance
of many new animal body plans about 530 million years ago. At this
time, at least nineteen, and perhaps as many as thirty-five phyla of
forty total (Meyer et al. 2003), made their first appearance on earth
within a narrow five- to ten-million-year window of geologic time
(Bowring et al. 1993, 1998a:1, 1998b:40; Kerr 1993; Monastersky 1993;
Aris-Brosou & Yang 2003). Many new subphyla, between 32 and 48 of 56
total (Meyer et al. 2003), and classes of animals also arose at this
time with representatives of these new higher taxa manifesting
significant morphological innovations. The Cambrian explosion thus
marked a major episode of morphogenesis in which many new and
disparate organismal forms arose in a geologically brief period of
time.
To say that the fauna of the Cambrian period appeared in a
geologically sudden manner also implies the absence of clear
transitional intermediate forms connecting Cambrian animals with
simpler pre-Cambrian forms. And, indeed, in almost all cases, the
Cambrian animals have no clear morphological antecedents in earlier
Vendian or Precambrian fauna (Miklos 1993, Erwin et al. 1997:132,
Steiner & Reitner 2001, Conway Morris 2003b:510, Valentine et al.
2003:519-520). Further, several recent discoveries and analyses
suggest that these morphological gaps may not be merely an artifact of
incomplete sampling of the fossil record (Foote 1997, Foote et al.
1999, Benton & Ayala 2003, Meyer et al. 2003), suggesting that the
fossil record is at least approximately reliable (Conway Morris 2003b:
505).
As a result, debate now exists about the extent to which this pattern
of evidence comports with a strictly monophyletic view of evolution
(Conway Morris 1998a, 2003a, 2003b:510; Willmer 1990, 2003). Further,
among those who accept a monophyletic view of the history of life,
debate exists about whether to privilege fossil or molecular data and
analyses. Those who think the fossil data provide a more reliable
picture of the origin of the Metazoan tend to think these animals
arose relatively quickly--that the Cambrian explosion had a “short
fuse.” (Conway Morris 2003b:505-506, Valentine & Jablonski 2003). Some
(Wray et al. 1996), but not all (Ayala et al. 1998), who think that
molecular phylogenies establish reliable divergence times from pre-
Cambrian ancestors think that the Cambrian animals evolved over a very
long period of time--that the Cambrian explosion had a “long fuse.”
This review will not address these questions of historical pattern.
Instead, it will analyze whether the neo-Darwinian process of mutation
and selection, or other processes of evolutionary change, can generate
the form and information necessary to produce the animals that arise
in the Cambrian. This analysis will, for the most part, 2 therefore,
not depend upon assumptions of either a long or short fuse for the
Cambrian explosion, or upon a monophyletic or polyphyletic view of the
early history of life.
Defining Biological Form and Information
Form, like life itself, is easy to recognize but often hard to define
precisely. Yet, a reasonable working definition of form will suffice
for our present purposes. Form can be defined as the four-dimensional
topological relations of anatomical parts. This means that one can
understand form as a unified arrangement of body parts or material
components in a distinct shape or pattern (topology)--one that exists
in three spatial dimensions and which arises in time during ontogeny.
Insofar as any particular biological form constitutes something like a
distinct arrangement of constituent body parts, form can be seen as
arising from constraints that limit the possible arrangements of
matter. Specifically, organismal form arises (both in phylogeny and
ontogeny) as possible arrangements of material parts are constrained
to establish a specific or particular arrangement with an identifiable
three dimensional topography--one that we would recognize as a
particular protein, cell type, organ, body plan or organism. A
particular “form,” therefore, represents a highly specific and
constrained arrangement of material components (among a much larger
set of possible arrangements).
Understanding form in this way suggests a connection to the notion of
information in its most theoretically general sense. When Shannon
(1948) first developed a mathematical theory of information he equated
the amount of information transmitted with the amount of uncertainty
reduced or eliminated in a series of symbols or characters.
Information, in Shannon's theory, is thus imparted as some options are
excluded and others are actualized. The greater the number of options
excluded, the greater the amount of information conveyed. Further,
constraining a set of possible material arrangements by whatever
process or means involves excluding some options and actualizing
others. Thus, to constrain a set of possible material states is to
generate information in Shannon's sense. It follows that the
constraints that produce biological form also imparted information. Or
conversely, one might say that producing organismal form by definition
requires the generation of information.
In classical Shannon information theory, the amount of information in
a system is also inversely related to the probability of the
arrangement of constituents in a system or the characters along a
communication channel (Shannon 1948). The more improbable (or complex)
the arrangement, the more Shannon information, or information-carrying
capacity, a string or system possesses.
Since the 1960s, mathematical biologists have realized that Shannon's
theory could be applied to the analysis of DNA and proteins to measure
the information-carrying capacity of these macromolecules. Since DNA
contains the assembly instructions for building proteins, the
information-processing system in the cell represents a kind of
communication channel (Yockey 1992:110). Further, DNA conveys
information via specifically arranged sequences of nucleotide bases.
Since each of the four bases has a roughly equal chance of occurring
at each site along the spine of the DNA molecule, biologists can
calculate the probability, and thus the information-carrying capacity,
of any particular sequence n bases long.
The ease with which information theory applies to molecular biology
has created confusion about the type of information that DNA and
proteins possess. Sequences of nucleotide bases in DNA, or amino acids
in a protein, are highly improbable and thus have large information-
carrying capacities. But, like meaningful sentences or lines of
computer code, genes and proteins are also specified with respect to
function. Just as the meaning of a sentence depends upon the specific
arrangement of the letters in a sentence, so too does the function of
a gene sequence depend upon the specific arrangement of the nucleotide
bases in a gene. Thus, molecular biologists beginning with Crick
equated information not only with complexity but also with
“specificity,” where “specificity” or “specified” has meant “necessary
to function” (Crick 1958:144, 153; Sarkar, 1996:191).3 Molecular
biologists such as Monod and Crick understood biological information--
the information stored in DNA and proteins--as something more than
mere complexity (or improbability). Their notion of information
associated both biochemical contingency and combinatorial complexity
with DNA sequences (allowing DNA's carrying capacity to be
calculated), but it also affirmed that sequences of nucleotides and
amino acids in functioning macromolecules possessed a high degree of
specificity relative to the maintenance of cellular function.
The ease with which information theory applies to molecular biology
has also created confusion about the location of information in
organisms. Perhaps because the information carrying capacity of the
gene could be so easily measured, it has been easy to treat DNA, RNA
and proteins as the sole repositories of biological information. Neo-
Darwinists in particular have assumed that the origination of
biological form could be explained by recourse to processes of genetic
variation and mutation alone (Levinton 1988:485). Yet if one
understands organismal form as resulting from constraints on the
possible arrangements of matter at many levels in the biological
hierarchy--from genes and proteins to cell types and tissues to organs
and body plans--then clearly biological organisms exhibit many levels
of information-rich structure.
Thus, we can pose a question, not only about the origin of genetic
information, but also about the origin of the information necessary to
generate form and structure at levels higher than that present in
individual proteins. We must also ask about the origin of the
“specified complexity,” as opposed to mere complexity, that
characterizes the new genes, proteins, cell types and body plans that
arose in the Cambrian explosion. Dembski (2002) has used the term
“complex specified information” (CSI) as a synonym for “specified
complexity” to help distinguish functional biological information from
mere Shannon information--that is, specified complexity from mere
complexity. This review will use this term as well.
The Cambrian Information Explosion
The Cambrian explosion represents a remarkable jump in the specified
complexity or “complex specified information” (CSI) of the biological
world. For over three billions years, the biological realm included
little more than bacteria and algae (Brocks et al. 1999). Then,
beginning about 570-565 million years ago (mya), the first complex
multicellular organisms appeared in the rock strata, including
sponges, cnidarians, and the peculiar Ediacaran biota (Grotzinger et
al. 1995). Forty million years later, the Cambrian explosion occurred
(Bowring et al. 1993). The emergence of the Ediacaran biota (570 mya),
and then to a much greater extent the Cambrian explosion (530 mya),
represented steep climbs up the biological complexity gradient.
One way to estimate the amount of new CSI that appeared with the
Cambrian animals is to count the number of new cell types that emerged
with them (Valentine 1995:91-93). Studies of modern animals suggest
that the sponges that appeared in the late Precambrian, for example,
would have required five cell types, whereas the more complex animals
that appeared in the Cambrian (e.g., arthropods) would have required
fifty or more cell types. Functionally more complex animals require
more cell types to perform their more diverse functions. New cell
types require many new and specialized proteins. New proteins, in
turn, require new genetic information. Thus an increase in the number
of cell types implies (at a minimum) a considerable increase in the
amount of specified genetic information. Molecular biologists have
recently estimated that a minimally complex single-celled organism
would require between 318 and 562 kilobase pairs of DNA to produce the
proteins necessary to maintain life (Koonin 2000). More complex single
cells might require upward of a million base pairs. Yet to build the
proteins necessary to sustain a complex arthropod such as a trilobite
would require orders of magnitude more coding instructions. The genome
size of a modern arthropod, the fruitfly Drosophila melanogaster, is
approximately 180 million base pairs (Gerhart & Kirschner 1997:121,
Adams et al. 2000). Transitions from a single cell to colonies of
cells to complex animals represent significant (and, in principle,
measurable) increases in CSI.
Building a new animal from a single-celled organism requires a vast
amount of new genetic information. It also requires a way of arranging
gene products--proteins--into higher levels of organization. New
proteins are required to service new cell types. But new proteins must
be organized into new systems within the cell; new cell types must be
organized into new tissues, organs, and body parts. These, in turn,
must be organized to form body plans. New animals, therefore, embody
hierarchically organized systems of lower-level parts within a
functional whole. Such hierarchical organization itself represents a
type of information, since body plans comprise both highly improbable
and functionally specified arrangements of lower-level parts. The
specified complexity of new body plans requires explanation in any
account of the Cambrian explosion.
Can neo-Darwinism explain the discontinuous increase in CSI that
appears in the Cambrian explosion--either in the form of new genetic
information or in the form of hierarchically organized systems of
parts? We will now examine the two parts of this question.
Novel Genes and Proteins
Many scientists and mathematicians have questioned the ability of
mutation and selection to generate information in the form of novel
genes and proteins. Such skepticism often derives from consideration
of the extreme improbability (and specificity) of functional genes and
proteins.
A typical gene contains over one thousand precisely arranged bases.
For any specific arrangement of four nucleotide bases of length n,
there is a corresponding number of possible arrangements of bases, 4n.
For any protein, there are 20n possible arrangements of protein-
forming amino acids. A gene 999 bases in length represents one of 4999
possible nucleotide sequences; a protein of 333 amino acids is one of
20333 possibilities.
Since the 1960s, some biologists have thought functional proteins to
be rare among the set of possible amino acid sequences. Some have used
an analogy with human language to illustrate why this should be the
case. Denton (1986, 309-311), for example, has shown that meaningful
words and sentences are extremely rare among the set of possible
combinations of English letters, especially as sequence length grows.
(The ratio of meaningful 12-letter words to 12-letter sequences is
1/1014, the ratio of 100-letter sentences to possible 100-letter
strings is 1/10100.) Further, Denton shows that most meaningful
sentences are highly isolated from one another in the space of
possible combinations, so that random substitutions of letters will,
after a very few changes, inevitably degrade meaning. Apart from a few
closely clustered sentences accessible by random substitution, the
overwhelming majority of meaningful sentences lie, probabilistically
speaking, beyond the reach of random search.
Denton (1986:301-324) and others have argued that similar constraints
apply to genes and proteins. They have questioned whether an
undirected search via mutation and selection would have a reasonable
chance of locating new islands of function--representing fundamentally
new genes or proteins--within the time available (Eden 1967,
Shutzenberger 1967, Lovtrup 1979). Some have also argued that
alterations in sequencing would likely result in loss of protein
function before fundamentally new function could arise (Eden 1967,
Denton 1986). Nevertheless, neither the extent to which genes and
proteins are sensitive to functional loss as a result of sequence
change, nor the extent to which functional proteins are isolated
within sequence space, has been fully known.
Recently, experiments in molecular biology have shed light on these
questions. A variety of mutagenesis techniques have shown that
proteins (and thus the genes that produce them) are indeed highly
specified relative to biological function (Bowie & Sauer 1989,
Reidhaar-Olson & Sauer 1990, Taylor et al. 2001). Mutagenesis research
tests the sensitivity of proteins (and, by implication, DNA) to
functional loss as a result of alterations in sequencing. Studies of
proteins have long shown that amino acid residues at many active
positions cannot vary without functional loss (Perutz & Lehmann 1968).
More recent protein studies (often using mutagenesis experiments) have
shown that functional requirements place significant constraints on
sequencing even at non-active site positions (Bowie & Sauer 1989,
Reidhaar-Olson & Sauer 1990, Chothia et al. 1998, Axe 2000, Taylor et
al. 2001). In particular, Axe (2000) has shown that multiple as
opposed to single position amino acid substitutions inevitably result
in loss of protein function, even when these changes occur at sites
that allow variation when altered in isolation. Cumulatively, these
constraints imply that proteins are highly sensitive to functional
loss as a result of alterations in sequencing, and that functional
proteins represent highly isolated and improbable arrangements of
amino acids -arrangements that are far more improbable, in fact, than
would be likely to arise by chance alone in the time available
(Reidhaar-Olson & Sauer 1990; Behe 1992; Kauffman 1995:44; Dembski
1998:175-223; Axe 2000, 2004). (See below the discussion of the
neutral theory of evolution for a precise quantitative assessment.)
Of course, neo-Darwinists do not envision a completely random search
through the set of all possible nucleotide sequences--so-called
“sequence space.” They envision natural selection acting to preserve
small advantageous variations in genetic sequences and their
corresponding protein products. Dawkins (1996), for example, likens an
organism to a high mountain peak. He compares climbing the sheer
precipice up the front side of the mountain to building a new organism
by chance. He acknowledges that his approach up “Mount Improbable”
will not succeed. Nevertheless, he suggests that there is a gradual
slope up the backside of the mountain that could be climbed in small
incremental steps. In his analogy, the backside climb up “Mount
Improbable” corresponds to the process of natural selection acting on
random changes in the genetic text. What chance alone cannot
accomplish blindly or in one leap, selection (acting on mutations) can
accomplish through the cumulative effect of many slight successive
steps.
Yet the extreme specificity and complexity of proteins presents a
difficulty, not only for the chance origin of specified biological
information (i.e., for random mutations acting alone), but also for
selection and mutation acting in concert. Indeed, mutagenesis
experiments cast doubt on each of the two scenarios by which neo-
Darwinists envisioned new information arising from the mutation/
selection mechanism (for review, see Lonnig 2001). For neo-Darwinism,
new functional genes either arise from non-coding sections in the
genome or from preexisting genes. Both scenarios are problematic.
In the first scenario, neo-Darwinists envision new genetic information
arising from those sections of the genetic text that can presumably
vary freely without consequence to the organism. According to this
scenario, non-coding sections of the genome, or duplicated sections of
coding regions, can experience a protracted period of “neutral
evolution” (Kimura 1983) during which alterations in nucleotide
sequences have no discernible effect on the function of the organism.
Eventually, however, a new gene sequence will arise that can code for
a novel protein. At that point, natural selection can favor the new
gene and its functional protein product, thus securing the
preservation and heritability of both.
This scenario has the advantage of allowing the genome to vary through
many generations, as mutations “search” the space of possible base
sequences. The scenario has an overriding problem, however: the size
of the combinatorial space (i.e., the number of possible amino acid
sequences) and the extreme rarity and isolation of the functional
sequences within that space of possibilities. Since natural selection
can do nothing to help generate new functional sequences, but rather
can only preserve such sequences once they have arisen, chance alone--
random variation--must do the work of information generation--that is,
of finding the exceedingly rare functional sequences within the set of
combinatorial possibilities. Yet the probability of randomly
assembling (or “finding,” in the previous sense) a functional sequence
is extremely small.
Cassette mutagenesis experiments performed during the early 1990s
suggest that the probability of attaining (at random) the correct
sequencing for a short protein 100 amino acids long is about 1 in 1065
(Reidhaar-Olson & Sauer 1990, Behe 1992:65-69). This result agreed
closely with earlier calculations that Yockey (1978) had performed
based upon the known sequence variability of cytochrome c in different
species and other theoretical considerations. More recent mutagenesis
research has provided additional support for the conclusion that
functional proteins are exceedingly rare among possible amino acid
sequences (Axe 2000, 2004). Axe (2004) has performed site directed
mutagenesis experiments on a 150-residue protein-folding domain within
a B-lactamase enzyme. His experimental method improves upon earlier
mutagenesis techniques and corrects for several sources of possible
estimation error inherent in them. On the basis of these experiments,
Axe has estimated the ratio of (a) proteins of typical size (150
residues) that perform a specified function via any folded structure
to (b) the whole set of possible amino acids sequences of that size.
Based on his experiments, Axe has estimated his ratio to be 1 to 1077.
Thus, the probability of finding a functional protein among the
possible amino acid sequences corresponding to a 150-residue protein
is similarly 1 in 1077.
Other considerations imply additional improbabilities. First, new
Cambrian animals would require proteins much longer than 100 residues
to perform many necessary specialized functions. Ohno (1996) has noted
that Cambrian animals would have required complex proteins such as
lysyl oxidase in order to support their stout body structures. Lysyl
oxidase molecules in extant organisms comprise over 400 amino acids.
These molecules are both highly complex (non-repetitive) and
functionally specified. Reasonable extrapolation from mutagenesis
experiments done on shorter protein molecules suggests that the
probability of producing functionally sequenced proteins of this
length at random is so small as to make appeals to chance absurd, even
granting the duration of the entire universe. (See Dembski
1998:175-223 for a rigorous calculation of this “Universal Probability
Bound”; See also Axe 2004.) Yet, second, fossil data (Bowring et al..
1993, 1998a:1, 1998b:40; Kerr 1993; Monatersky 1993), and even
molecular analyses supporting deep divergence (Wray et al. 1996),
suggest that the duration of the Cambrian explosion (between 5-10 x
106 and, at most, 7 x 107 years) is far smaller than that of the
entire universe (1.3-2 x 1010 years). Third, DNA mutation rates are
far too low to generate the novel genes and proteins necessary to
building the Cambrian animals, given the most probable duration of the
explosion as determined by fossil studies (Conway Morris 1998b). As
Ohno (1996:8475) notes, even a mutation rate of 10-9 per base pair per
year results in only a 1% change in the sequence of a given section of
DNA in 10 million years. Thus, he argues that mutational divergence of
preexisting genes cannot explain the origin of the Cambrian forms in
that time.4
The selection/mutation mechanism faces another probabilistic obstacle.
The animals that arise in the Cambrian exhibit structures that would
have required many new types of cells, each of which would have
required many novel proteins to perform their specialized functions.
Further, new cell types require Asystems of proteins that must, as a
condition of functioning, act in close coordination with one another.
The unit of selection in such systems ascends to the system as a
whole. Natural selection selects for functional advantage. But new
cell types require whole systems of proteins to perform their
distinctive functions. In such cases, natural selection cannot
contribute to the process of information generation until after the
information necessary to build the requisite system of proteins has
arisen. Thus random variations must, again, do the work of information
generation--and now not simply for one protein, but for many proteins
arising at nearly the same time. Yet the odds of this occurring by
chance alone are, of course, far smaller than the odds of the chance
origin of a single gene or protein--so small in fact as to render the
chance origin of the genetic information necessary to build a new cell
type (a necessary but not sufficient condition of building a new body
plan) problematic given even the most optimistic estimates for the
duration of the Cambrian explosion.
Dawkins (1986:139) has noted that scientific theories can rely on only
so much “luck” before they cease to be credible. The neutral theory of
evolution, which, by its own logic, prevents natural selection from
playing a role in generating genetic information until after the fact,
relies on entirely too much luck. The sensitivity of proteins to
functional loss, the need for long proteins to build new cell types
and animals, the need for whole new systems of proteins to service new
cell types, the probable brevity of the Cambrian explosion relative to
mutation rates--all suggest the immense improbability (and
implausibility) of any scenario for the origination of Cambrian
genetic information that relies upon random variation alone unassisted
by natural selection.
Yet the neutral theory requires novel genes and proteins to arise--
essentially--by random mutation alone. Adaptive advantage accrues
after the generation of new functional genes and proteins. Thus,
natural selection cannot play a role until new information-bearing
molecules have independently arisen. Thus neutral theorists envisioned
the need to scale the steep face of a Dawkins-style precipice of which
there is no gradually sloping backside--a situation that, by Dawkins'
own logic, is probabilistically untenable.
In the second scenario, neo-Darwinists envisioned novel genes and
proteins arising by numerous successive mutations in the preexisting
genetic text that codes for proteins. To adapt Dawkins's metaphor,
this scenario envisions gradually climbing down one functional peak
and then ascending another. Yet mutagenesis experiments again suggest
a difficulty. Recent experiments show that, even when exploring a
region of sequence space populated by proteins of a single fold and
function, most multiple-position changes quickly lead to loss of
function (Axe 2000). Yet to turn one protein into another with a
completely novel structure and function requires specified changes at
many sites. Indeed, the number of changes necessary to produce a new
protein greatly exceeds the number of changes that will typically
produce functional losses. Given this, the probability of escaping
total functional loss during a random search for the changes needed to
produce a new function is extremely small--and this probability
diminishes exponentially with each additional requisite change (Axe
2000). Thus, Axe's results imply that, in all probability, random
searches for novel proteins (through sequence space) will result in
functional loss long before any novel functional protein will emerge.
Blanco et al. have come to a similar conclusion. Using directed
mutagenesis, they have determined that residues in both the
hydrophobic core and on the surface of the protein play essential
roles in determining protein structure. By sampling intermediate
sequences between two naturally occurring sequences that adopt
different folds, they found that the intermediate sequences “lack a
well defined three-dimensional structure.” Thus, they conclude that it
is unlikely that a new protein fold via a series of folded
intermediates sequences (Blanco et al. 1999:741).
Thus, although this second neo-Darwinian scenario has the advantage of
starting with functional genes and proteins, it also has a lethal
disadvantage: any process of random mutation or rearrangement in the
genome would in all probability generate nonfunctional intermediate
sequences before fundamentally new functional genes or proteins would
arise. Clearly, nonfunctional intermediate sequences confer no
survival advantage on their host organisms. Natural selection favors
only functional advantage. It cannot select or favor nucleotide
sequences or polypeptide chains that do not yet perform biological
functions, and still less will it favor sequences that efface or
destroy preexisting function.
Evolving genes and proteins will range through a series of
nonfunctional intermediate sequences that natural selection will not
favor or preserve but will, in all probability, eliminate (Blanco et
al. 1999, Axe 2000). When this happens, selection-driven evolution
will cease. At this point, neutral evolution of the genome (unhinged
from selective pressure) may ensue, but, as we have seen, such a
process must overcome immense probabilistic hurdles, even granting
cosmic time.
Thus, whether one envisions the evolutionary process beginning with a
noncoding region of the genome or a preexisting functional gene, the
functional specificity and complexity of proteins impose very
stringent limitations on the efficacy of mutation and selection. In
the first case, function must arise first, before natural selection
can act to favor a novel variation. In the second case, function must
be continuously maintained in order to prevent deleterious (or lethal)
consequences to the organism and to allow further evolution. Yet the
complexity and functional specificity of proteins implies that both
these conditions will be extremely difficult to meet. Therefore, the
neo-Darwinian mechanism appears to be inadequate to generate the new
information present in the novel genes and proteins that arise with
the Cambrian animals.
Novel Body Plans
The problems with the neo-Darwinian mechanism run deeper still. In
order to explain the origin of the Cambrian animals, one must account
not only for new proteins and cell types, but also for the origin of
new body plans. Within the past decade, developmental biology has
dramatically advanced our understanding of how body plans are built
during ontogeny. In the process, it has also uncovered a profound
difficulty for neo-Darwinism.
Significant morphological change in organisms requires attention to
timing. Mutations in genes that are expressed late in the development
of an organism will not affect the body plan. Mutations expressed
early in development, however, could conceivably produce significant
morphological change (Arthur 1997:21). Thus, events expressed early in
the development of organisms have the only realistic chance of
producing large-scale macroevolutionary change (Thomson 1992). As John
and Miklos (1988:309) explain, macroevolutionary change requires
alterations in the very early stages of ontogenesis.
Yet recent studies in developmental biology make clear that mutations
expressed early in development typically have deleterious effects
(Arthur 1997:21). For example, when early-acting body plan molecules,
or morphogens such as bicoid (which helps to set up the anterior-
posterior head-to-tail axis in Drosophila), are perturbed, development
shuts down (Nusslein-Volhard & Wieschaus 1980, Lawrence & Struhl 1996,
Muller & Newman 2003).5 The resulting embryos die. Moreover, there is
a good reason for this. If an engineer modifies the length of the
piston rods in an internal combustion engine without modifying the
crankshaft accordingly, the engine won't start. Similarly, processes
of development are tightly integrated spatially and temporally such
that changes early in development will require a host of other
coordinated changes in separate but functionally interrelated
developmental processes downstream. For this reason, mutations will be
much more likely to be deadly if they disrupt a functionally deeply-
embedded structure such as a spinal column than if they affect more
isolated anatomical features such as fingers (Kauffman 1995:200).
This problem has led to what McDonald (1983) has called “a great
Darwinian paradox” (p. 93). McDonald notes that genes that are
observed to vary within natural populations do not lead to major
adaptive changes, while genes that could cause major changes--the very
stuff of macroevolution--apparently do not vary. In other words,
mutations of the kind that macroevolution doesn't need (namely, viable
genetic mutations in DNA expressed late in development) do occur, but
those that it does need (namely, beneficial body plan mutations
expressed early in development) apparently don't occur.6 According to
Darwin (1859:108) natural selection cannot act until favorable
variations arise in a population. Yet there is no evidence from
developmental genetics that the kind of variations required by neo-
Darwinism--namely, favorable body plan mutations--ever occur.
Developmental biology has raised another formidable problem for the
mutation/selection mechanism. Embryological evidence has long shown
that DNA does not wholly determine morphological form (Goodwin 1985,
Nijhout 1990, Sapp 1987, Muller & Newman 2003), suggesting that
mutations in DNA alone cannot account for the morphological changes
required to build a new body plan.
DNA helps direct protein synthesis.7 It also helps to regulate the
timing and expression of the synthesis of various proteins within
cells. Yet, DNA alone does not determine how individual proteins
assemble themselves into larger systems of proteins; still less does
it solely determine how cell types, tissue types, and organs arrange
themselves into body plans (Harold 1995:2774, Moss 2004). Instead,
other factors--such as the three-dimensional structure and
organization of the cell membrane and cytoskeleton and the spatial
architecture of the fertilized egg--play important roles in
determining body plan formation during embryogenesis.
For example, the structure and location of the cytoskeleton influence
the patterning of embryos. Arrays of microtubules help to distribute
the essential proteins used during development to their correct
locations in the cell. Of course, microtubules themselves are made of
many protein subunits. Nevertheless, like bricks that can be used to
assemble many different structures, the tubulin subunits in the cell's
microtubules are identical to one another. Thus, neither the tubulin
subunits nor the genes that produce them account for the different
shape of microtubule arrays that distinguish different kinds of
embryos and developmental pathways. Instead, the structure of the
microtubule array itself is determined by the location and arrangement
of its subunits, not the properties of the subunits themselves. For
this reason, it is not possible to predict the structure of the
cytoskeleton of the cell from the characteristics of the protein
constituents that form that structure (Harold 2001:125).
Two analogies may help further clarify the point. At a building site,
builders will make use of many materials: lumber, wires, nails,
drywall, piping, and windows. Yet building materials do not determine
the floor plan of the house, or the arrangement of houses in a
neighborhood. Similarly, electronic circuits are composed of many
components, such as resistors, capacitors, and transistors. But such
lower-level components do not determine their own arrangement in an
integrated circuit. Biological symptoms also depend on hierarchical
arrangements of parts. Genes and proteins are made from simple
building blocks--nucleotide bases and amino acids--arranged in
specific ways. Cell types are made of, among other things, systems of
specialized proteins. Organs are made of specialized arrangements of
cell types and tissues. And body plans comprise specific arrangements
of specialized organs. Yet, clearly, the properties of individual
proteins (or, indeed, the lower-level parts in the hierarchy
generally) do not fully determine the organization of the higher-level
structures and organizational patterns (Harold 2001:125). It follows
that the genetic information that codes for proteins does not
determine these higher-level structures either.
These considerations pose another challenge to the sufficiency of the
neo-Darwinian mechanism. Neo-Darwinism seeks to explain the origin of
new information, form, and structure as a result of selection acting
on randomly arising variation at a very low level within the
biological hierarchy, namely, within the genetic text. Yet major
morphological innovations depend on a specificity of arrangement at a
much higher level of the organizational hierarchy, a level that DNA
alone does not determine. Yet if DNA is not wholly responsible for
body plan morphogenesis, then DNA sequences can mutate indefinitely,
without regard to realistic probabilistic limits, and still not
produce a new body plan. Thus, the mechanism of natural selection
acting on random mutations in DNA cannot in principle generate novel
body plans, including those that first arose in the Cambrian
explosion.
Of course, it could be argued that, while many single proteins do not
by themselves determine cellular structures and/or body plans,
proteins acting in concert with other proteins or suites of proteins
could determine such higher-level form. For example, it might be
pointed out that the tubulin subunits (cited above) are assembled by
other helper proteins--gene products--called Microtubule Associated
Proteins (MAPS). This might seem to suggest that genes and gene
products alone do suffice to determine the development of the three-
dimensional structure of the cytoskeleton.
Yet MAPS, and indeed many other necessary proteins, are only part of
the story. The location of specified target sites on the interior of
the cell membrane also helps to determine the shape of the
cytoskeleton. Similarly, so does the position and structure of the
centrosome which nucleates the microtubules that form the
cytoskeleton. While both the membrane targets and the centrosomes are
made of proteins, the location and form of these structures is not
wholly determined by the proteins that form them. Indeed, centrosome
structure and membrane patterns as a whole convey three-dimensional
structural information that helps determine the structure of the
cytoskeleton and the location of its subunits (McNiven & Porter
1992:313-329). Moreover, the centrioles that compose the centrosomes
replicate independently of DNA replication (Lange et al. 2000:235-249,
Marshall & Rosenbaum 2000:187-205). The daughter centriole receives
its form from the overall structure of the mother centriole, not from
the individual gene products that constitute it (Lange et al. 2000).
In ciliates, microsurgery on cell membranes can produce heritable
changes in membrane patterns, even though the DNA of the ciliates has
not been altered (Sonneborn 1970:1-13, Frankel 1980:607-623; Nanney
1983:163-170). This suggests that membrane patterns (as opposed to
membrane constituents) are impressed directly on daughter cells. In
both cases, form is transmitted from parent three-dimensional
structures to daughter three-dimensional structures directly and is
not wholly contained in constituent proteins or genetic information
(Moss 2004).
Thus, in each new generation, the form and structure of the cell
arises as the result of both gene products and preexisting three-
dimensional structure and organization. Cellular structures are built
from proteins, but proteins find their way to correct locations in
part because of preexisting three-dimensional patterns and
organization inherent in cellular structures. Preexisting three-
dimensional form present in the preceding generation (whether inherent
in the cell membrane, the centrosomes, the cytoskeleton or other
features of the fertilized egg) contributes to the production of form
in the next generation. Neither structural proteins alone, nor the
genes that code for them, are sufficient to determine the three-
dimensional shape and structure of the entities they form. Gene
products provide necessary, but not sufficient conditions, for the
development of three-dimensional structure within cells, organs and
body plans (Harold 1995:2767). But if this is so, then natural
selection acting on genetic variation alone cannot produce the new
forms that arise in history of life.
Self-Organizational Models
Of course, neo-Darwinism is not the only evolutionary theory for
explaining the origin of novel biological form. Kauffman (1995) doubts
the efficacy of the mutation/selection mechanism. Nevertheless, he has
advanced a self-organizational theory to account for the emergence of
new form, and presumably the information necessary to generate it.
Whereas neo-Darwinism attempts to explain new form as the consequence
of selection acting on random mutation, Kauffman suggests that
selection acts, not mainly on random variations, but on emergent
patterns of order that self-organize via the laws of nature.
Kauffman (1995:47-92) illustrates how this might work with various
model systems in a computer environment. In one, he conceives a system
of buttons connected by strings. Buttons represent novel genes or gene
products; strings represent the law-like forces of interaction that
obtain between gene products-i.e., proteins. Kauffman suggests that
when the complexity of the system (as represented by the number of
buttons and strings) reaches a critical threshold, new modes of
organization can arise in the system “for free”--that is, naturally
and spontaneously--after the manner of a phase transition in
chemistry.
Another model that Kauffman develops is a system of interconnected
lights. Each light can flash in a variety of states--on, off,
twinkling, etc. Since there is more than one possible state for each
light, and many lights, there are a vast number of possible states
that the system can adopt. Further, in his system, rules determine how
past states will influence future states. Kauffman asserts that, as a
result of these rules, the system will, if properly tuned, eventually
produce a kind of order in which a few basic patterns of light
activity recur with greater-than-random frequency. Since these actual
patterns of light activity represent a small portion of the total
number of possible states in which the system can reside, Kauffman
seems to imply that self-organizational laws might similarly result in
highly improbable biological outcomes--perhaps even sequences (of
bases or amino acids) within a much larger sequence space of
possibilities.
Do these simulations of self-organizational processes accurately model
the origin of novel genetic information? It is hard to think so.
First, in both examples, Kauffman presupposes but does not explain
significant sources of preexisting information. In his buttons-and-
strings system, the buttons represent proteins, themselves packets of
CSI, and the result of preexisting genetic information. Where does
this information come from? Kauffman (1995) doesn't say, but the
origin of such information is an essential part of what needs to be
explained in the history of life. Similarly, in his light system, the
order that allegedly arises for “for free” actually arises only if the
programmer of the model system “tunes” it in such a way as to keep it
from either (a) generating an excessively rigid order or (b)
developing into chaos (pp. 86-88). Yet this necessary tuning involves
an intelligent programmer selecting certain parameters and excluding
others--that is, inputting information.
Second, Kauffman's model systems are not constrained by functional
considerations and thus are not analogous to biological systems. A
system of interconnected lights governed by pre-programmed rules may
well settle into a small number of patterns within a much larger space
of possibilities. But because these patterns have no function, and
need not meet any functional requirements, they have no specificity
analogous to that present in actual organisms. Instead, examination of
Kauffman's (1995) model systems shows that they do not produce
sequences or systems characterized by specified complexity, but
instead by large amounts of symmetrical order or internal redundancy
interspersed with aperiodicity or (mere) complexity (pp. 53, 89, 102).
Getting a law-governed system to generate repetitive patterns of
flashing lights, even with a certain amount of variation, is clearly
interesting, but not biologically relevant. On the other hand, a
system of lights flashing the title of a Broadway play would model a
biologically relevant self-organizational process, at least if such a
meaningful or functionally specified sequence arose without
intelligent agents previously programming the system with equivalent
amounts of CSI. In any case, Kauffman's systems do not produce
specified complexity, and thus do not offer promising models for
explaining the new genes and proteins that arose in the Cambrian.
Even so, Kauffman suggests that his self-organizational models can
specifically elucidate aspects of the Cambrian explosion. According to
Kauffman (1995:199-201), new Cambrian animals emerged as the result of
“long jump” mutations that established new body plans in a discrete
rather than gradual fashion. He also recognizes that mutations
affecting early development are almost inevitably harmful. Thus, he
concludes that body plans, once established, will not change, and that
any subsequent evolution must occur within an established body plan
(Kauffman 1995:201). And indeed, the fossil record does show a curious
(from a neo-Darwinian point of view) top-down pattern of appearance,
in which higher taxa (and the body plans they represent) appear first,
only later to be followed by the multiplication of lower taxa
representing variations within those original body designs (Erwin et
al. 1987, Lewin 1988, Valentine & Jablonski 2003:518). Further, as
Kauffman expects, body plans appear suddenly and persist without
significant modification over time.
But here, again, Kauffman begs the most important question, which is:
what produces the new Cambrian body plans in the first place? Granted,
he invokes “long jump mutations” to explain this, but he identifies no
specific self-organizational process that can produce such mutations.
Moreover, he concedes a principle that undermines the plausibility of
his own proposal. Kauffman acknowledges that mutations that occur
early in development are almost inevitably deleterious. Yet
developmental biologists know that these are the only kind of
mutations that have a realistic chance of producing large-scale
evolutionary change--i.e., the big jumps that Kauffman invokes. Though
Kauffman repudiates the neo-Darwinian reliance upon random mutations
in favor of self-organizing order, in the end, he must invoke the most
implausible kind of random mutation in order to provide a self-
organizational account of the new Cambrian body plans. Clearly, his
model is not sufficient.
Punctuated Equilibrium
Of course, still other causal explanations have been proposed. During
the 1970s, the paleontologists Eldredge and Gould (1972) proposed the
theory of evolution by punctuated equilibrium in order to account for
a pervasive pattern of “sudden appearance” and “stasis” in the fossil
record. Though advocates of punctuated equilibrium were mainly seeking
to describe the fossil record more accurately than earlier gradualist
neo-Darwinian models had done, they did also propose a mechanism--
known as species selection--by which the large morphological jumps
evident in fossil record might have been produced. According to
punctuationalists, natural selection functions more as a mechanism for
selecting the fittest species rather than the most-fit individual
among a species. Accordingly, on this model, morphological change
should occur in larger, more discrete intervals than it would given a
traditional neo-Darwinian understanding.
Despite its virtues as a descriptive model of the history of life,
punctuated equilibrium has been widely criticized for failing to
provide a mechanism sufficient to produce the novel form
characteristic of higher taxonomic groups. For one thing, critics have
noted that the proposed mechanism of punctuated evolutionary change
simply lacked the raw material upon which to work. As Valentine and
Erwin (1987) note, the fossil record fails to document a large pool of
species prior to the Cambrian. Yet the proposed mechanism of species
selection requires just such a pool of species upon which to act.
Thus, they conclude that the mechanism of species selection probably
does not resolve the problem of the origin of the higher taxonomic
groups (p. 96).8 Further, punctuated equilibrium has not addressed the
more specific and fundamental problem of explaining the origin of the
new biological information (whether genetic or epigenetic) necessary
to produce novel biological form. Advocates of punctuated equilibrium
might assume that the new species (upon which natural selection acts)
arise by known microevolutionary processes of speciation (such as
founder effect, genetic drift or bottleneck effect) that do not
necessarily depend upon mutations to produce adaptive changes. But, in
that case, the theory lacks an account of how the specifically higher
taxa arise. Species selection will only produce more fit species. On
the other hand, if punctuationalists assume that processes of genetic
mutation can produce more fundamental morphological changes and
variations, then their model becomes subject to the same problems as
neo-Darwinism (see above). This dilemma is evident in Gould (2002:710)
insofar as his attempts to explain adaptive complexity inevitably
employ classical neo-Darwinian modes of explanation.9
Structuralism
Another attempt to explain the origin of form has been proposed by the
structuralists such as Gerry Webster and Brian Goodwin (1984, 1996).
These biologists, drawing on the earlier work of D'Arcy Thompson
(1942), view biological form as the result of structural constraints
imposed upon matter by morphogenetic rules or laws. For reasons
similar to those discussed above, the structuralists have insisted
that these generative or morphogenetic rules do not reside in the
lower level building materials of organisms, whether in genes or
proteins. Webster and Goodwin (1984:510-511) further envisioned
morphogenetic rules or laws operating ahistorically, similar to the
way in which gravitational or electromagnetic laws operate. For this
reason, structuralists see phylogeny as of secondary importance in
understanding the origin of the higher taxa, though they think that
transformations of form can occur. For structuralists, constraints on
the arrangement of matter arise not mainly as the result of historical
contingencies--such as environmental changes or genetic mutations--but
instead because of the continuous ahistorical operation of fundamental
laws of form--laws that organize or inform matter.
While this approach avoids many of the difficulties currently
afflicting neo-Darwinism (in particular those associated with its
“genocentricity”), critics (such as Maynard Smith 1986) of
structuralism have argued that the structuralist explanation of form
lacks specificity. They note that structuralists have been unable to
say just where laws of form reside--whether in the universe, or in
every possible world, or in organisms as a whole, or in just some part
of organisms. Further, according to structuralists, morphogenetic laws
are mathematical in character. Yet, structuralists have yet to specify
the mathematical formulae that determine biological forms.
Others (Yockey 1992; Polanyi 1967, 1968; Meyer 2003) have questioned
whether physical laws could in principle generate the kind of
complexity that characterizes biological systems. Structuralists
envision the existence of biological laws that produce form in much
the same way that physical laws produce form. Yet the forms that
physicists regard as manifestations of underlying laws are
characterized by large amounts of symmetric or redundant order, by
relatively simple patterns such as vortices or gravitational fields or
magnetic lines of force. Indeed, physical laws are typically expressed
as differential equations (or algorithms) that almost by definition
describe recurring phenomena--patterns of compressible “order” not
“complexity” as defined by algorithmic information theory (Yockey
1992:77-83). Biological forms, by contrast, manifest greater
complexity and derive in ontogeny from highly complex initial
conditions--i.e., non-redundant sequences of nucleotide bases in the
genome and other forms of information expressed in the complex and
irregular three-dimensional topography of the organism or the
fertilized egg. Thus, the kind of form that physical laws produce is
not analogous to biological form--at least not when compared from the
standpoint of (algorithmic) complexity. Further, physical laws lack
the information content to specify biology systems. As Polyanyi (1967,
1968) and Yockey (1992:290) have shown, the laws of physics and
chemistry allow, but do not determine, distinctively biological modes
of organization. In other words, living systems are consistent with,
but not deducible, from physical-chemical laws (1992:290).
Of course, biological systems do manifest some reoccurring patterns,
processes and behaviors. The same type of organism develops repeatedly
from similar ontogenetic processes in the same species. Similar
processes of cell division reoccur in many organisms. Thus, one might
describe certain biological processes as law-governed. Even so, the
existence of such biological regularities does not solve the problem
of the origin of form and information, since the recurring processes
described by such biological laws (if there be such laws) only occur
as the result of preexisting stores of (genetic and/or epigenetic)
information and these information-rich initial conditions impose the
constraints that produce the recurring behavior in biological systems.
(For example, processes of cell division recur with great frequency in
organisms, but depend upon information-rich DNA and proteins
molecules.) In other words, distinctively biological regularities
depend upon preexisting biological information. Thus, appeals to
higher-level biological laws presuppose, but do not explain, the
origination of the information necessary to morphogenesis.
Thus, structuralism faces a difficult in principle dilemma. On the one
hand, physical laws produce very simple redundant patterns that lack
the complexity characteristic of biological systems. On the other
hand, distinctively biological laws--if there are such laws--depend
upon preexisting information-rich structures. In either case, laws are
not good candidates for explaining the origination of biological form
or the information necessary to produce it.
Cladism: An Artifact of Classification?
Some cladists have advanced another approach to the problem of the
origin of form, specifically as it arises in the Cambrian. They have
argued that the problem of the origin of the phyla is an artifact of
the classification system, and therefore, does not require
explanation. Budd and Jensen (2000), for example, argue that the
problem of the Cambrian explosion resolves itself if one keeps in mind
the cladistic distinction between “stem” and “crown” groups. Since
crown groups arise whenever new characters are added to simpler more
ancestral stem groups during the evolutionary process, new phyla will
inevitably arise once a new stem group has arisen. Thus, for Budd and
Jensen what requires explanation is not the crown groups corresponding
to the new Cambrian phyla, but the earlier more primitive stem groups
that presumably arose deep in the Proterozoic. Yet since these earlier
stem groups are by definition less derived, explaining them will be
considerably easier than explaining the origin of the Cambrian animals
de novo. In any case, for Budd and Jensen the explosion of new phyla
in the Cambrian does not require explanation. As they put it, “given
that the early branching points of major clades is an inevitable
result of clade diversification, the alleged phenomenon of the phyla
appearing early and remaining morphologically static is not seen to
require particular explanation” (Budd & Jensen 2000:253).
While superficially plausible, perhaps, Budd and Jensen's attempt to
explain away the Cambrian explosion begs crucial questions. Granted,
as new characters are added to existing forms, novels morphology and
greater morphological disparity will likely result. But what causes
new characters to arise? And how does the information necessary to
produce new characters originate? Budd and Jensen do not specify. Nor
can they say how derived the ancestral forms are likely to have been,
and what processes, might have been sufficient to produce them.
Instead, they simply assume the sufficiency of known neo-Darwinian
mechanisms (Budd & Jensen 2000:288). Yet, as shown above, this
assumption is now problematic. In any case, Budd and Jensen do not
explain what causes the origination of biological form and
information.
Convergence and Teleological Evolution
More recently, Conway Morris (2000, 2003c) has suggested another
possible explanation based on the tendency for evolution to converge
on the same structural forms during the history of life. Conway Morris
cites numerous examples of organisms that possess very similar forms
and structures, even though such structures are often built from
different material substrates and arise (in ontogeny) by the
expression of very different genes. Given the extreme improbability of
the same structures arising by random mutation and selection in
disparate phylogenies, Conway Morris argues that the pervasiveness of
convergent structures suggests that evolution may be in some way
“channeled” toward similar functional and/or structural endpoints.
Such an end-directed understanding of evolution, he admits, raises the
controversial prospect of a teleological or purposive element in the
history of life. For this reason, he argues that the phenomenon of
convergence has received less attention than it might have otherwise.
Nevertheless, he argues that just as physicists have reopened the
question of design in their discussions of anthropic fine-tuning, the
ubiquity of convergent structures in the history of life has led some
biologists (Denton 1998) to consider extending teleological thinking
to biology. And, indeed, Conway Morris himself intimates that the
evolutionary process might be “underpinned by a purpose” (2000:8,
2003b:511).
Conway Morris, of course, considers this possibility in relation to a
very specific aspect of the problem of organismal form, namely, the
problem of explaining why the same forms arise repeatedly in so many
disparate lines of decent. But this raises a question. Could a similar
approach shed explanatory light on the more general causal question
that has been addressed in this review? Could the notion of purposive
design help provide a more adequate explanation for the origin of
organismal form generally? Are there reasons to consider design as an
explanation for the origin of the biological information necessary to
produce the higher taxa and their corresponding morphological novelty?
The remainder of this review will suggest that there are such reasons.
In so doing, it may also help explain why the issue of teleology or
design has reemerged within the scientific discussion of biological
origins (Denton 1986, 1998; Thaxton et al. 1992; Kenyon & Mills 1996:
Behe 1996, 2004; Dembski 1998, 2002, 2004; Conway Morris 2000, 2003a,
2003b, Lonnig 2001; Lonnig & Saedler 2002; Nelson & Wells 2003; Meyer
2003, 2004; Bradley 2004) and why some scientists and philosophers of
science have considered teleological explanations for the origin of
form and information despite strong methodological prohibitions
against design as a scientific hypothesis (Gillespie 1979, Lenior
1982:4).
First, the possibility of design as an explanation follows logically
from a consideration of the deficiencies of neo-Darwinism and other
current theories as explanations for some of the more striking
“appearances of design” in biological systems. Neo-Darwinists such as
Ayala (1994:5), Dawkins (1986:1), Mayr (1982:xi-xii) and Lewontin
(1978) have long acknowledged that organisms appear to have been
designed. Of course, neo-Darwinists assert that what Ayala (1994:5)
calls the “obvious design” of living things is only apparent since the
selection/mutation mechanism can explain the origin of complex form
and organization in living systems without an appeal to a designing
agent. Indeed, neo-Darwinists affirm that mutation and selection--and
perhaps other similarly undirected mechanisms--are fully sufficient to
explain the appearance of design in biology. Self-organizational
theorists and punctuationalists modify this claim, but affirm its
essential tenet. Self-organization theorists argue that natural
selection acting on self organizing order can explain the complexity
of living things--again, without any appeal to design.
Punctuationalists similarly envision natural selection acting on newly
arising species with no actual design involved.
And clearly, the neo-Darwinian mechanism does explain many appearances
of design, such as the adaptation of organisms to specialized
environments that attracted the interest of 19th century biologists.
More specifically, known microevolutionary processes appear quite
sufficient to account for changes in the size of Galapagos finch beaks
that have occurred in response to variations in annual rainfall and
available food supplies (Weiner 1994, Grant 1999).
But does neo-Darwinism, or any other fully materialistic model,
explain all appearances of design in biology, including the body plans
and information that characterize living systems? Arguably, biological
forms--such as the structure of a chambered nautilus, the organization
of a trilobite, the functional integration of parts in an eye or
molecular machine--attract our attention in part because the organized
complexity of such systems seems reminiscent of our own designs. Yet,
this review has argued that neo-Darwinism does not adequately account
for the origin of all appearances of design, especially if one
considers animal body plans, and the information necessary to
construct them, as especially striking examples of the appearance of
design in living systems. Indeed, Dawkins (1995:11) and Gates
(1996:228) have noted that genetic information bears an uncanny
resemblance to computer software or machine code. For this reason, the
presence of CSI in living organisms, and the discontinuous increases
of CSI that occurred during events such as the Cambrian explosion,
appears at least suggestive of design.
Does neo-Darwinism or any other purely materialistic model of
morphogenesis account for the origin of the genetic and other forms of
CSI necessary to produce novel organismal form? If not, as this review
has argued, could the emergence of novel information-rich genes,
proteins, cell types and body plans have resulted from actual design,
rather than a purposeless process that merely mimics the powers of a
designing intelligence? The logic of neo-Darwinism, with its specific
claim to have accounted for the appearance of design, would itself
seem to open the door to this possibility. Indeed, the historical
formulation of Darwinism in dialectical opposition to the design
hypothesis (Gillespie 1979), coupled with the neo-Darwinism's
inability to account for many salient appearances of design including
the emergence of form and information, would seem logically to reopen
the possibility of actual (as opposed to apparent) design in the
history of life.
A second reason for considering design as an explanation for these
phenomena follows from the importance of explanatory power to
scientific theory evaluation and from a consideration of the potential
explanatory power of the design hypothesis. Studies in the methodology
and philosophy of science have shown that many scientific theories,
particularly in the historical sciences, are formulated and justified
as inferences to the best explanation (Lipton 1991:32-88, Brush
1989:1124-1129, Sober 2000:44). Historical scientists, in particular,
assess or test competing hypotheses by evaluating which hypothesis
would, if true, provide the best explanation for some set of relevant
data (Meyer 1991, 2002; Cleland 2001:987-989, 2002:474-496).10 Those
with greater explanatory power are typically judged to be better, more
probably true, theories. Darwin (1896:437) used this method of
reasoning in defending his theory of universal common descent.
Moreover, contemporary studies on the method of “inference to the best
explanation” have shown that determining which among a set of
competing possible explanations constitutes the best depends upon
judgments about the causal adequacy, or “causal powers,” of competing
explanatory entities (Lipton 1991:32-88). In the historical sciences,
uniformitarian and/or actualistic (Gould 1965, Simpson 1970, Rutten
1971, Hooykaas 1975) canons of method suggest that judgments about
causal adequacy should derive from our present knowledge of cause and
effect relationships. For historical scientists, “the present is the
key to the past” means that present experience-based knowledge of
cause and effect relationships typically guides the assessment of the
plausibility of proposed causes of past events.
Yet it is precisely for this reason that current advocates of the
design hypothesis want to reconsider design as an explanation for the
origin of biological form and information. This review, and much of
the literature it has surveyed, suggests that four of the most
prominent models for explaining the origin of biological form fail to
provide adequate causal explanations for the discontinuous increases
of CSI that are required to produce novel morphologies. Yet, we have
repeated experience of rational and conscious agents--in particular
ourselves--generating or causing increases in complex specified
information, both in the form of sequence-specific lines of code and
in the form of hierarchically arranged systems of parts.
In the first place, intelligent human agents--in virtue of their
rationality and consciousness--have demonstrated the power to produce
information in the form of linear sequence-specific arrangements of
characters. Indeed, experience affirms that information of this type
routinely arises from the activity of intelligent agents. A computer
user who traces the information on a screen back to its source
invariably comes to a mind--that of a software engineer or programmer.
The information in a book or inscriptions ultimately derives from a
writer or scribe--from a mental, rather than a strictly material,
cause. Our experience-based knowledge of information-flow confirms
that systems with large amounts of specified complexity (especially
codes and languages) invariably originate from an intelligent source
from a mind or personal agent. As Quastler (1964) put it, the
“creation of new information is habitually associated with conscious
activity” (p. 16). Experience teaches this obvious truth.
Further, the highly specified hierarchical arrangements of parts in
animal body plans also suggest design, again because of our experience
of the kinds of features and systems that designers can and do
produce. At every level of the biological hierarchy, organisms require
specified and highly improbable arrangements of lower-level
constituents in order to maintain their form and function. Genes
require specified arrangements of nucleotide bases; proteins require
specified arrangements of amino acids; new cell types require
specified arrangements of systems of proteins; body plans require
specialized arrangements of cell types and organs. Organisms not only
contain information-rich components (such as proteins and genes), but
they comprise information-rich arrangements of those components and
the systems that comprise them. Yet we know, based on our present
experience of cause and effect relationships, that design engineers--
possessing purposive intelligence and rationality--have the ability to
produce information-rich hierarchies in which both individual modules
and the arrangements of those modules exhibit complexity and
specificity--information so defined. Individual transistors,
resistors, and capacitors exhibit considerable complexity and
specificity of design; at a higher level of organization, their
specific arrangement within an integrated circuit represents
additional information and reflects further design. Conscious and
rational agents have, as part of their powers of purposive
intelligence, the capacity to design information-rich parts and to
organize those parts into functional information-rich systems and
hierarchies. Further, we know of no other causal entity or process
that has this capacity. Clearly, we have good reason to doubt that
mutation and selection, self-organizational processes or laws of
nature, can produce the information-rich components, systems, and body
plans necessary to explain the origination of morphological novelty
such as that which arises in the Cambrian period.
There is a third reason to consider purpose or design as an
explanation for the origin of biological form and information:
purposive agents have just those necessary powers that natural
selection lacks as a condition of its causal adequacy. At several
points in the previous analysis, we saw that natural selection lacked
the ability to generate novel information precisely because it can
only act after new functional CSI has arisen. Natural selection can
favor new proteins, and genes, but only after they perform some
function. The job of generating new functional genes, proteins and
systems of proteins therefore falls entirely to random mutations. Yet
without functional criteria to guide a search through the space of
possible sequences, random variation is probabilistically doomed. What
is needed is not just a source of variation (i.e., the freedom to
search a space of possibilities) or a mode of selection that can
operate after the fact of a successful search, but instead a means of
selection that (a) operates during a search--before success--and that
(b) is guided by information about, or knowledge of, a functional
target.
Demonstration of this requirement has come from an unlikely quarter:
genetic algorithms. Genetic algorithms are programs that allegedly
simulate the creative power of mutation and selection. Dawkins and
Kuppers, for example, have developed computer programs that putatively
simulate the production of genetic information by mutation and natural
selection (Dawkins 1986:47-49, Kuppers 1987:355-369). Nevertheless, as
shown elsewhere (Meyer 1998:127-128, 2003:247-248), these programs
only succeed by the illicit expedient of providing the computer with a
“target sequence” and then treating relatively greater proximity to
future function (i.e., the target sequence), not actual present
function, as a selection criterion. As Berlinski (2000) has argued,
genetic algorithms need something akin to a “forward looking memory”
in order to succeed. Yet such foresighted selection has no analogue in
nature. In biology, where differential survival depends upon
maintaining function, selection cannot occur before new functional
sequences arise. Natural selection lacks foresight.
What natural selection lacks, intelligent selection--purposive or goal-
directed design--provides. Rational agents can arrange both matter and
symbols with distant goals in mind. In using language, the human mind
routinely “finds” or generates highly improbable linguistic sequences
to convey an intended or preconceived idea. In the process of thought,
functional objectives precede and constrain the selection of words,
sounds and symbols to generate functional (and indeed meaningful)
sequences from among a vast ensemble of meaningless alternative
combinations of sound or symbol (Denton 1986:309-311). Similarly, the
construction of complex technological objects and products, such as
bridges, circuit boards, engines and software, result from the
application of goal-directed constraints (Polanyi 1967, 1968). Indeed,
in all functionally integrated complex systems where the cause is
known by experience or observation, design engineers or other
intelligent agents applied boundary constraints to limit possibilities
in order to produce improbable forms, sequences or structures.
Rational agents have repeatedly demonstrated the capacity to constrain
the possible to actualize improbable but initially unrealized future
functions. Repeated experience affirms that intelligent agents (minds)
uniquely possess such causal powers.
Analysis of the problem of the origin of biological information,
therefore, exposes a deficiency in the causal powers of natural
selection that corresponds precisely to powers that agents are
uniquely known to possess. Intelligent agents have foresight. Such
agents can select functional goals before they exist. They can devise
or select material means to accomplish those ends from among an array
of possibilities and then actualize those goals in accord with a
preconceived design plan or set of functional requirements. Rational
agents can constrain combinatorial space with distant outcomes in
mind. The causal powers that natural selection lacks--almost by
definition--are associated with the attributes of consciousness and
rationality--with purposive intelligence. Thus, by invoking design to
explain the origin of new biological information, contemporary design
theorists are not positing an arbitrary explanatory element
unmotivated by a consideration of the evidence. Instead, they are
positing an entity possessing precisely the attributes and causal
powers that the phenomenon in question requires as a condition of its
production and explanation.
Conclusion
An experience-based analysis of the causal powers of various
explanatory hypotheses suggests purposive or intelligent design as a
causally adequate--and perhaps the most causally adequate--explanation
for the origin of the complex specified information required to build
the Cambrian animals and the novel forms they represent. For this
reason, recent scientific interest in the design hypothesis is
unlikely to abate as biologists continue to wrestle with the problem
of the origination of biological form and the higher taxa.
Literature Cited
Adams, M. D. Et alia. 2000. The genome sequence of Drosophila
melanogaster.--Science 287:2185-2195.
Aris-Brosou, S., & Z. Yang. 2003. Bayesian models of episodic
evolution support a late Precambrian explosive diversification of the
Metazoa.--Molecular Biology and Evolution 20:1947-1954.
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.
______. 2004. 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 Kingdom.
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, United Kingdom.
Benton, M., & F. J. Ayala. 2003. Dating the tree of life--Science
300:1698-1700.
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 261:1293-1298.
______. 1998a. A new look at evolutionary rates in deep time: Uniting
paleontology and high-precision geochronology.--GSA Today 8:1-8.
______. 1998b. Geochronology comes of age.--Geotimes 43:36-40.
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 Kingdom.
Brocks, J. J., G. A. Logan, R. Buick, & R. E. Summons. 1999. Archean
molecular fossils and the early rise of eukaryotes.--Science
285:1033-1036.
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 75:253-295.
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 29:987-990.
______. 2002. Methodological and epistemic differences between
historical science and experimental science.--Philosophy of Science
69:474-496.
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 Biology 21:1-9.
______. 1998b. Early Metazoan evolution: Reconciling paleontology and
molecular biology.--American Zoologist 38 (1998):867-877.
______. 2000. Evolution: bringing molecules into the fold.--Cell
100:1-11.
______. 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 47(7-8):505-515.
______. 2003c. Life's solution: inevitable humans in a lonely
universe. Cambridge University Press, Cambridge, United Kingdom.
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 York.
Dawkins, R. 1986. The blind watchmaker. Penguin Books, London, United
Kingdom.
______. 1995. River out of Eden. Basic Books, New York.
______. 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, United Kingdom.
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 York.
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 38:281-294.
______. 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.
______, J. Valentine, & D. Jablonski. 1997. The origin of animal body
plans.--American Scientist 85:126-137.
______, ______, & J. J. Sepkoski. 1987. A comparative study of
diversification events: the early Paleozoic versus the Mesozoic.--
Evolution 41:1177-1186.
Foote, M. 1997. Sampling, taxonomic description, and our evolving
knowledge of morphological diversity.--Paleobiology 23:181-206.
______, 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 283:1310-1314.
Frankel, J. 1980. Propagation of cortical differences in tetrahymena.--
Genetics 94:607-623.
Gates, B. 1996. The road ahead. Blue Penguin, Boulder, Colorado.
Gerhart, J., & M. Kirschner. 1997. Cells, embryos, and evolution.
Blackwell Science, London, United Kingdom.
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, Chicago.
Goodwin, B. C. 1985. What are the causes of morphogenesis?--BioEssays
3:32-36.
______. 1995. How the leopard changed its spots: the evolution of
complexity. Scribner's, New York, New York.
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, Switzerland.
Grotzinger, J. P., S. A. Bowring, B. Z. Saylor, & A. J. Kaufman. 1995.
Biostratigraphic and geochronologic constraints on early animal
evolution.--Science 270:598-604.
Harold, F. M. 1995. From morphogenes to morphogenesis.--Microbiology
141:2765-2778.
______. 2001. The way of the cell: molecules, organisms, and the order
of life. Oxford University Press, New York.
Hodge, M. J. S. 1977. The structure and strategy of Darwin's long
argument.--British Journal for the History of Science 10:237-245.
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 17(1):9-16.
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 Kingdom.
Koonin, E. 2000. How many genes can make a cell?: the minimal genome
concept.--Annual Review of Genomics and Human Genetics 1:99-116.
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.
Lawrence, P. A., & G. Struhl. 1996. Morphogens, compartments and
pattern: lessons from Drosophila?--Cell 85:951-961.
Lenior, T. 1982. The strategy of life. University of Chicago Press,
Chicago.
Levinton, J. 1988. Genetics, paleontology, and macroevolution.
Cambridge University Press, Cambridge, United Kingdom.
______. 1992. The big bang of animal evolution.--Scientific American
267:84-91.
Lewin, R. 1988. A lopsided look at evolution.--Science 241:292.
Lewontin, R. 1978. Adaptation. Pp. 113-125 in Evolution: a Scientific
American book. W. H. Freeman & Company, San Francisco.
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, New York.
______, & H. Saedler. 2002. Chromosome rearrangements and transposable
elements.--Annual Review of Genetics 36:389-410.
Lovtrup, S. 1979. Semantics, logic and vulgate neo-darwinism.--
Evolutionary Theory 4:157-172.
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.
Maynard 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 Systematics 14:77-102.
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 Kingdom.
______. 1998. DNA by design: an inference to the best explanation for
the origin of biological information.--Rhetoric & Public Affairs, 1(4):
519-555.
______. 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 Francisco.
______. 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. Palaeontols, 15:7-41.
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
Heredity, 74:163-170.
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.
Nijhout, H. F. 1990. Metaphors and the role of genes in development.--
BioEssays 12:441-446.
Nusslein-Volhard, C., & E. Wieschaus. 1980. Mutations affecting
segment number and polarity in Drosophila.--Nature 287:795-801.
Ohno, S. 1996. The notion of the Cambrian pananimalia genome.--
Proceedings of the National Academy of Sciences, U.S.A. 93:8475-8478.
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 219:902-909.
Polanyi, M. 1967. Life transcending physics and chemistry.--Chemical
and Engineering News, 45(35):54-66.
______. 1968. Life's irreducible structure.--Science 160:1308-1312,
especially p. 1309.
Pourquie, O. 2003. Vertebrate somitogenesis: a novel paradigm for
animal segmentation?--International Journal of Developmental Biology 47
(7-8):597-603.
Quastler, H. 1964. The emergence of biological organization. Yale
University Press, New Haven, Connecticut.
Raff, R. 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, 7:306-316.
Rutten, M. G. 1971. The origin of life by natural causes. Elsevier,
Amsterdam.
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.
Shu, 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 China.--Nature 402:42-46.
Shubin, N. H., & C. R. Marshall. 2000. Fossils, genes, and the origin
of novelty. Pp. 324-340 in Deep time. The Paleontological Society.
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 Francisco.
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 Biology 213:241-274.
Steiner, M., & R. Reitner. 2001. Evidence of organic structures in
Ediacara-type fossils and associated microbial mats.--Geology 29(12):
1119-1122.
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. 98:10596-10601.
Thaxton, C. B., W. L. Bradley, & R. L. Olsen. 1992. The mystery of
life's origin: reassessing current theories. Lewis and Stanley,
Dallas, Texas.
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 32:106-112.
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 47:517-522.
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.)
291:305-309.
______, & 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 77:503-10.
______, & ______. 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 Kingdom.
______. 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.
Woese, 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 Kingdom.
End Notes
1 Specifically, Gilbert et al. (1996) argued that changes in
morphogenetic fields might produce large-scale changes in the
developmental programs and, ultimately, body plans of organisms. Yet
they offered no evidence that such fields--if indeed they exist--can
be altered to produce advantageous variations in body plan, though
this is a necessary condition of any successful causal theory of
macroevolution.
2 If one takes the fossil record at face value and assumes that the
Cambrian explosion took place within a relatively narrow 5-10 million
year window, explaining the origin of the information necessary to
produce new proteins, for example, becomes more acute in part because
mutation rates would not have been sufficient to generate the number
of changes in the genome necessary to build the new proteins for more
complex Cambrian animals (Ohno 1996:8475-8478). This review will argue
that, even if one allows several hundred million years for the origin
of the metazoan, significant probabilistic and other difficulties
remain with the neo-Darwinian explanation of the origin of form and
information.
3 As Crick put it, “information means here the precise determination
of sequence, either of bases in the nucleic acid or on amino acid
residues in the protein” (Crick 1958:144, 153).
4 To solve this problem Ohno himself proposes the existence of a
hypothetical ancestral form that possessed virtually all the genetic
information necessary to produce the new body plans of the Cambrian
animals. He asserts that this ancestor and its “pananimalian genome”
might have arisen several hundred million years before the Cambrian
explosion. On this view, each of the different Cambrian animals would
have possessed virtually identical genomes, albeit with considerable
latent and unexpressed capacity in the case of each individual form
(Ohno 1996:8475-8478). While this proposal might help explain the
origin of the Cambrian animal forms by reference to preexisting
genetic information, it does not solve, but instead merely displaces,
the problem of the origin of the genetic information necessary to
produce these new forms.
5 Some have suggested that mutations in “master regulator” Hox genes
might provide the raw material for body plan morphogenesis. Yet there
are two problems with this proposal. First, Hox gene expression begins
only after the foundation of the body plan has been established in
early embryogenesis. (Davidson 2001:66). Second, Hox genes are highly
conserved across many disparate phyla and so cannot account for the
morphological differences that exist between the phyla (Valentine
2004:88).
6 Notable differences in the developmental pathways of similar
organisms have been observed. For example, congeneric species of sea
urchins (from genus Heliocidaris) exhibit striking differences in
their developmental pathways (Raff 1999:110-121). Thus, it might be
argued that such differences show that early developmental programs
can in fact be mutated to produce new forms. Nevertheless, there are
two problems with this claim. First, there is no direct evidence that
existing differences in sea urchin development arose by mutation.
Second, the observed differences in the developmental programs of
different species of sea urchins do not result in new body plans, but
instead in highly conserved structures. Despite differences in
developmental patterns, the endpoints are the same. Thus, even if it
can be assumed that mutations produced the differences in
developmental pathways, it must be acknowledged that such changes did
not result in novel form.
7 Of course, many post-translation processes of modification also play
a role in producing a functional protein. Such processes make it
impossible to predict a protein's final sequencing from its
corresponding gene sequence alone (Sarkar 1996:199-202).
8 Erwin (2004:21), although friendly to the possibility of species
selection, argues that Gould provides little evidence for its
existence. “The difficulty” writes Erwin of species selection, “...is
that we must rely on Gould's arguments for theoretical plausibility
and sufficient relative frequency. Rarely is a mass of data presented
to justify and support Gould's conclusion.” Indeed, Gould (2002)
himself admitted that species selection remains largely a hypothetical
construct: “I freely admit that well-documented cases of species
selection do not permeate the literature” (p. 710).
9”I do not deny either the wonder, or the powerful importance, of
organized adaptive complexity. I recognize that we know no mechanism
for the origin of such organismal features other than conventional
natural selection at the organismic level--for the sheer intricacy and
elaboration of good biomechanical design surely precludes either
random production, or incidental origin as a side consequence of
active processes at other levels” (Gould 2002:710). “Thus, we do not
challenge the efficacy or the cardinal importance of organismal
selection. As previously discussed, I fully agree with Dawkins (1986)
and others that one cannot invoke a higher-level force like species
selection to explain 'things that organisms do'--in particular, the
stunning panoply of organismic adaptations that has always motivated
our sense of wonder about the natural world, and that Darwin (1859)
described, in one of his most famous lines (3), as 'that perfection of
structure and coadaptation which most justly excites our
admiration'“ (Gould 2002:886).
10 Theories in the historical sciences typically make claims about
what happened in the past, or what happened in the past to cause
particular events to occur (Meyer 1991:57-72). For this reason,
historical scientific theories are rarely tested by making predictions
about what will occur under controlled laboratory conditions (Cleland
2001:987, 2002:474-496). Instead, such theories are usually tested by
comparing their explanatory power against that of their competitors
with respect to already known facts. Even in the case in which
historical theories make claims about past causes they usually do so
on the basis of preexisting knowledge of cause and effect
relationships. Nevertheless, prediction may play a limited role in
testing historical scientific theories since such theories may have
implications as to what kind of evidence is likely to emerge in the
future. For example, neo-Darwinism affirms that new functional
sections of the genome arise by trial and error process of mutation
and subsequent selection. For this reason, historically many neo-
Darwinists expected or predicted that the large non-coding regions of
the genome--so-called “junk DNA”--would lack function altogether
(Orgel & Crick 1980). On this line of thinking, the nonfunctional
sections of the genome represent nature's failed experiments that
remain in the genome as a kind of artifact of the past activity of the
mutation and selection process. Advocates of the design hypotheses on
the other hand, would have predicted that non-coding regions of the
genome might well reveal hidden functions, not only because design
theorists do not think that new genetic information arises by a trial
and error process of mutation and selection, but also because designed
systems are often functionally polyvalent. Even so, as new studies
reveal more about the functions performed by the non-coding regions of
the genome (Gibbs 2003), the design hypothesis can no longer be said
to make this claim in the form of a specifically future-oriented
prediction. Instead, the design hypothesis might be said to gain
confirmation or support from its ability to explain this now known
evidence, albeit after the fact. Of course, neo Darwinists might also
amend their original prediction using various auxiliary hypotheses to
explain away the presence of newly discovered functions in the non-
coding regions of DNA. In both cases, considerations of ex post facto
explanatory power reemerge as central to assessing and testing
competing historical theories.
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