A Concept in Crisis
Before Darwin, homology was defined morphologically and explained by reference to ideal
archetypes -- that is, to intelligent design. Darwin reformulated biology in naturalistic*
rather than teleological terms, and explained homology as the result of descent with
modification from a common ancestor. Descent with modification, however, renders design
unnecessary only if it is due entirely to naturalistic mechanisms. Two such mechanisms
have been proposed, genetic programs and developmental pathways, but neither one fits the
evidence. Without an empirically demonstrated naturalistic mechanism to account for
homology, design remains a possibility which can only be excluded on the basis of
questionable philosophical assumptions.
* In this article, "naturalism" and "naturalistic" refer to the
philosophical doctrine that nature is the whole of reality, and that intelligent causation
does not qualify as a scientific explanation.
Morphological and Pyhlogenetic Homology
From at least the time of Aristotle, people who study living organisms have noted some
remarkable similarities among very diverse creatures. Bats and butterflies are quite
different from each other, yet both have wings to fly; bats fly and whales swim, yet the
bones in a bat's wing and a whale's flipper are strikingly alike. The first kind of
similarity involves different structures which perform the same function, and in 1843
anatomist Richard Owen called this "analogy." In contrast, the second kind of
similarity involves similar structures which perform different functions, and Owen called
this "homology." Owen (and other pre-Darwinian biologists) attributed homology
to the existence of archetypes: biological structures are similar because they conform
more or less to pre-existing patterns. (Bowler, 1989; Panchen, 1994)
In 1859, Charles Darwin offered a different explanation for homology. According to
Darwin, bats and whales possess similar bone structures because they inherited them from a
common ancestor, not because they were constructed according to the same archetype. By
replacing archetypes (which imply design and intelligent causation) with a natural
mechanism such as common descent, Darwin hoped to render idealistic explanations
unnecessary and to place biology on a securely naturalistic basis.
Not all structural similarities, however, are inherited from a common ancestor (as
Darwin and his followers recognized). For example, the eye of a mouse is structurally
similar to the eye of an octopus, yet their supposed common ancestor did not possess such
an eye. In 1870, Ray Lankester coined the term "homoplasy" to describe such
features. Implicit in this distinction was a new definition of homology. As evolutionary
biologist Ernst Mayr put it, after Darwin the "biologically most meaningful
definition" of homology was: "A feature in two or more taxa is homologous when
it is derived from the same (or a corresponding) feature of their common ancestor."
(Mayr, 1982) In other words, what Darwin proposed as the explanation for homology
became its definition. For many biologists, the post-Darwinian (or phylogenetic)
definition of homology has replaced the structural (or morphological) definition. (Hall,
1992; Panchen, 1994)
Darwin's reform -- explaining homology by material descent with modification -- was
incorporated into the neo-Darwinian synthesis of the mid-twentieth century with the
discovery of the mechanisms of transmission genetics (i.e., inheritence), about which
Darwin knew nothing. Figure 1
displays a flow diagram with the key elements of the neo-Darwinian explanation of
homology. The cardinal "explainer" (so to speak), or cause, which Darwin
advocated classically in chapter XIII of the Origin of Species, is material
descent. Every organism in our experience has at least one parent. Thus, humans (for
instance) possess two large bones, the radius and the ulna, in their forelimb because, by
hypothesis, their distant non-human primate ancestors also possessed two such bones,
albeit with slightly different shapes -- and so on, back to the primary progenitor which
first evolved the radius-ulna pattern.
Neo-Darwinian biologists added to this the new causal dimension of the physical basis
of heredity. In brief, at reproduction, each parent (in a sexually-reproducing species)
passes half of its genetic material (DNA) to its offspring. What descends from generation
to generation, therefore, are genes: DNA. These genes, in turn control the processes of
development in the fertilized egg, as the phenotype (adult morphology) is being
constructed. Evolution, or the adaptive modification of adult form, occurs because genes
are subject to mutation. These mutations affect development; and differing phenotypes are
constructed among the offspring, which are then selected by their ability to compete and
This explanation has a beautiful plausibility. It is also in very serious trouble.
Within the past decade or so, a flood of new data on the genetic constituents of
development, as well as the revisiting of older but still unsolved puzzles (see below),
have battered the foundations of the neo-Darwinian explanation of homology. In a recent
commentary on the troubled state of the concept, David Cannatella, of the Department of
Zoology at the University of Texas wrote:
... Wake (1994) offered that homology is the central concept of all biology. If this is
true, then a large group of comparative biologists lacks a guiding principle. Onedoes not
have to look far to see that homology (and therefore homoplasy) is not understood by many
biologists. (Cannatella 1997, 369)
In this article we review in broad outline some of the major difficulties with the
neo-Darwinian explanation of homology, in particular, the incongruent causal relationship
between genes, development, and phenotypic form. Despite the standard textbook claims,
homology has never been adequately explained by neo-Darwinism. The time is ripe, we
contend, to reconsider biology's exclusion of intelligent design as a possible cause.
The Need for a Naturalistic Mechanism
Ask your neighborhood evolutionary biologist how he knows intelligent design is
unnecessary to explain homology, and odds are he will say something like, "Well, we
have a demonstrated natural mechanism which accounts for the phenomenon." In
actuality, however, the mechanism has not been demonstrated; rather, homology is simply
taken as prima facie evidence of descent, and design is excluded out of hand. The
problem is unintentionally illustrated by biologist Tim Berra in his 1990 book, Evolution
and the Myth of Creationism (Stanford University Press). According to Berra, "If
you look at a 1953 Corvette and compare it to the latest model, only the most general
resemblances are evident, but if you compare a 1953 and a 1954 Corvette, side by side,
then a 1954 and a 1955 model, and so on, the descent with modification is overwhelmingly
obvious. This is what paleontologists do with fossils, and the evidence is so solid and
comprehensive that it cannot be denied by reasonable people." (p. 117)
As the title of his book indicates, Berra's primary purpose is to show that living
organisms are the result of naturalistic evolution rather than intelligent design.
Structural similarities among automobiles, however, even similarities between older and
newer models (which Berra calls "descent with modification") are due to
construction according to pre-existing patterns, i.e., to design. Ironically, therefore,
Berra's analogy shows that even striking similarities are not sufficient to exclude
design-based explanations. In order to demonstrate naturalistic evolution, it is necessary
to show that the mechanism by which organisms are constructed (unlike the mechanism by
which automobiles are constructed) does not involve design.
One could simply postulate that the mechanism of biological evolution is naturalistic,
arguing that the postulate is justified because science is limited to studying natural
mechanisms. Although such a philosophical move may seem very reasonable, it gravely
compromises the status of evolutionary biology as an objective science. Asserting that
something is objectively true implies that it is based on empirical evidence, not merely
assumed a priori on philosophical grounds. A methodological exclusion of
design-based explanations constitutes a limitation on one's science, not a description of
objective reality. If evolutionary biologists want to show that the actual mechanism of
evolution does not involve intelligent design, they cannot merely exclude the possibility a
priori, but must take the more difficult approach of proposing and corroborating a
This alternative must account naturalistically for what evolutionary biologist Leigh
Van Valen has called "continuity of information." (Van Valen, 1982) According to
Van Valen, homologous features are produced during the development of each individual
organism by information which has been inherited, with modification, from the organism's
ancestors. Thus the first step toward understanding the mechanism of evolution would be to
determine the nature of the information which controls the development of the embryo.
Homology and Genetics
One possibility is that this information is encoded in the organism's genes. In the
1930's, the synthesis of Darwin's theory and population genetics explained evolution as a
change in gene frequencies, and several decades later the discovery of the structure and
function of DNA extended this explanation to the molecular level.
According to the neo-Darwinian synthesis, a genetic program encoded in DNA directs
embryonic development; the process of reproduction transmits this program to subsequent
generations, but mutations in the DNA sometimes modify it ("descent with
modification"); thus descendants of the original organism may possess structures
which are similar but not identical ("homologies") (See Fig. 1). No design is
required, so the explanation is thoroughly naturalistic. By 1970, molecular biologist
Jacques Monod felt justified in announcing that "the mechanism of Darwinism is at
last securely founded," and that as a consequence "man has to understand that he
is a mere accident." (quoted in Judson, 1980, p. 217)
Efforts to correlate major phenotypic evolution with changes in gene frequencies,
however, have not been very successful. Detailed studies at the molecular level fail to
demonstrate the expected correspondence between changes in gene products and the sorts of
organismal changes which constitute the "stuff of evolution." (Lewontin, 1974,
p. 160). According to Rudolf Raff and Thomas Kaufman, evolution by DNA mutations "is
largely uncoupled from morphological evolution;" the "most spectacular"
example of this is the morphological dissimilarity of humans and chimpanzees despite a 99%
similarity in their DNA. (Raff and Kaufman, 1983, pp. 67, 78).
Some biologists have proposed that the remaining 1% consists of "regulatory
genes" which have such profound effects on development that a few mutations in them
could account for dramatic differences. For example, mutations in homeotic genes can
transform a fly's antenna into a leg, or produce two pairs of wings where there would
normally be only one, or cause eyes to develop on a fly's leg. Furthermore, genes similar
to the homeotic genes of flies have been found in most other types of animals, including
mammals. Based on the profound developmental effects and almost universal occurrence of
such genes, biologist Eric Davidson and his colleagues recently wrote that "novel
morphological forms in animal evolution result from changes in genetically encoded
programs of developmental regulation." (Davidson et al., 1995, p. 1319)
According to this view, homologous features are programmed by similar genes. Assuming
that genes with similar sequences are unlikely to originate independently through random
mutations, sequence similarity would indicate common ancestry. Features produced by
similar sequences could then be inferred to be phylogenetically homologous.
The very universality of homeotic genes, however, raises a serious problem for this
view. Although mice have a gene very similar to the one that can transform a fly's antenna
into a leg (Antennapedia), mice do not have antennae, and their corresponding gene
affects the hindbrain; and although mice and flies share a similar gene which affects eye
development (eyeless), the fly's multifaceted eye is profoundly different from a mouse's
camera-like eye. In both cases (Antennapedia and eyeless), similar homeotic genes
affect the development of structures which are non-homologous by either the classical
morphological definition or the post-Darwinian phylogenetic definition. If similar genes
can "determine" such radically different structures, then those genes aren't
really determining structure at all. Instead, they appear to be functioning as binary
switches between alternate developmental fates, with the information for the resulting
structures residing elsewhere. (Wells, 1996)
Not only are non-homologous structures produced by organisms with supposedly homologous
genes, but organisms with different genes can also produce similar structures. The most
famous examples involves the genes, mentioned above, which affect wing and eye development
in flies. Fly embryos with a normal gene for wing development, when treated with ether,
can be induced to grow a second pair, just as though they possessed the mutant form of the
gene (For a review, see Hall, 1992). Flies with a mutant form of the eye gene fail to
develop eyes; but if eyeless flies are bred for many generations, some of their
descendants will develop eyes even though they still possess the mutant form of the gene.
Such anomalies led embryologist Gavin de Beer to conclude that "homologous structures
need not be controlled by identical genes," and that "the inheritance of
homologous structures from a common ancestor ... cannot be ascribed to identity of
genes." (de Beer, 1971, pp. 15-16)
The underlying assumption that a genetic program directs embryonic development has been
seriously questioned by developmental biologists (For a review, see Wells, 1992). Sydney
Brenner, who originally proposed genetic programs in 1970, repudiated the idea when he
realized that the information required to specify the neural connections of even a simple
worm far exceeds the information content of its DNA. (Brenner, 1973) A decade later,
developmental biologist Brian Goodwin noted that "genes are responsible for
determining which molecules an organism can produce," but "the molecular
composition of organisms does not, in general, determine their form." (Goodwin, 1985,
p. 32) And in a 1990 critique of the notion of genetic programs, H.F. Nijhout concluded
that "the only strictly correct view of the function of genes is that they supply
cells, and ultimately organisms, with chemical materials." (Nijhout, 1990, p. 444)
Clearly, the genetic explanation for homology is inadequate. As an alternative, some
biologists have suggested that homology results from complex developmental mechanisms
which are not reducible to a genetic program.
Homology and Developmental Pathways
Since homologies cannot be explained by equating developmental information with DNA
sequences, some biologists have attempted to explain it by attributing it to similar
developmental pathways. Although DNA determines the amino acid sequence of proteins
essential for development, such pathways also involve other factors, such as the
localization of cytoplasmic constituents in the egg cell, physical constraints resulting
from the size of the embryo, and so on. (Wells, 1992)
Efforts to correlate homology with developmental pathways, however, have been uniformly
unsuccessful. First, similar developmental pathways may produce very dissimilar features.
At the molecular level, it is well known that virtually identical inducers may participate
in the development of non-homologous structures in different animals. (Gilbert, 1994) At
the multicellular level, the pattern of embryonic cell movements which generates body form
in birds also generates body form in a few species of frogs. (Elinson, 1987) And even at
the organismal level, morphologically indistinguishable larvae may develop into completely
different species. (de Beer, 1958) Clearly, similar developmental pathways may produce
Second, and more dramatically, similar features are often produced by very different
developmental pathways. No one doubts that the gut is homologous throughout the
vertebrates, yet the gut forms from different embryonic cells in different vertebrates.
The neural tube, embryonic precursor of the spinal cord, is regarded as homologous
throughout the chordates, yet in some its formation depends on induction by the underlying
notochord while in others it does not. (Gilbert, 1994) Evidently, "structures can owe
their origin to different methods of induction without forfeiting their homology."
(de Beer, 1958, p. 151) Indeed, as developmental biologist Pere Alberch noted in 1985, it
is "the rule rather than the exception" that "homologous structures form
from distinctly dissimilar initial states" (see Figure 2). (Alberch, 1985, p.
Production of similar forms from dissimilar pathways is also common at later stages of
development. Many types of animals pass through a larval stage on their way to adulthood,
a phenomenon known as indirect development. For example, most frogs begin life as swimming
tadpoles, and only later metamorphose into four-legged animals. There are many species of
frogs, however, which bypass the larval stage and develop directly. Remarkably, the adults
of some of these direct developers are almost indistinguishable from the adults of sister
species which develop indirectly. In other words, very similar frogs can be produced by
direct and indirect development, even though the pathways are obviously radically
different. The same phenomenon is common among sea urchins and ascidians (see Figure 3). (Raff, 1996)
Even the classic example of vertebrate limbs shows that homology cannot be explained by
similarities in developmental pathways. Skeletal patterns in vertebrate limbs are
initially laid down in the form of cartilage condensations, which later ossify into bone.
The sequence of cartilage condensation is the developmental pathway which determines the
future pattern of bones in the limb. Yet similar bone patterns in different species (i.e.,
homologies) arise from different sequences of cartilage condensation. (Shubin, 1991) In
the words of biologist Richard Hinchliffe: "Embryology does not contribute to
comparative morphology by providing evidence of limb homology in the form of an unchanging
pattern of condensation common to all tetrapod limbs." (Hinchliffe, 1990, p. 121)
The constancy of final patterns despite varying pathways has prompted developmental
biologist GŁnter Wagner to suggest that homology might be due to conserved developmental
"constraints". (Wagner, 1989) Wagner's critics, however, object that this notion
is too vague to be useful. Although developmental constraints emphasize the fact that
embryos are capable of producing similar end-points by a variety of routes, they do not
constitute a naturalistic mechanism accessible to empirical investigation.
So embryology has not solved the problem of homology. In 1958, Gavin de Beer observed that
"correspondence between homologous structures cannot be pressed back to similarity of
position of the cells in the embryo, or of the parts of the egg out of which the
structures are ultimately composed, or of developmental mechanisms by which they are
formed." (de Beer, 1958, p. 152) Subsequent research has overwhelmingly confirmed the
correctness of de Beer's observation. Homology, whether defined morphologically or
phylogenetically, cannot be attributed to similar developmental pathways any more than it
can be attributed to similar genes. So far, the naturalistic mechanisms proposed to
explain homology do not fit the evidence.
In 1802, William Paley wrote that someone crossing a heath and finding a stone could
reasonably attribute its presence to purposeless natural causes. Upon finding a watch,
however, and seeing that "its several parts are framed and put together for a
purpose," one could conclude that the watch had been designed. By analogy, Paley
argued, one could also conclude that living things are designed. (Paley, 1802, p. 2) In
1859, Charles Darwin argued that living things are more like Paley's stone than Paley's
watch, and claimed that everything which Paley attributed to design could be accounted for
naturalistically, by descent with modification.
As Berra's automobile analogy shows, however, descent with modification is not enough
to exclude design. It is necessary, in addition, to show that the mechanism of descent
with modification is thoroughly naturalistic. Darwin thought he had done this with his
theory of natural selection, but as the problem of homology demonstrates, he failed to
accomplish his goal.
Diverse organisms possess homologous features. Homology in some cases may or may not be
due to inheritance from a common ancestor, but it is definitely not due to similarity of
genes or similarity of developmental pathways. In 1971, Gavin de Beer wrote: "What
mechanism can it be that results in the production of homologous organs, the same
'patterns', in spite of their not being controlled by the same genes? I asked this
question in 1938, and it has not been answered." (de Beer, 1971, p.16) Twenty-six
years later, the question still has not been answered.
Without a naturalistic mechanism to account for homology, however, Darwinian evolution
cannot claim to have demonstrated scientifically that living things are undesigned, and
the possibility remains that homologies are patterned after non-material archetypes.
Without a demonstrated mechanism, naturalistic biologists are left with only one
alternative: exclude design a priori, on philosophical grounds.
This exclusion could be taken as a statement that intelligent design does not exist, or
it could be taken as a statement that intelligent design is beyond the reach of empirical
science. The first is a philosophical or theological statement, and warrants the same
response. The second is a methodological limitation which cannot be logically extrapolated
to a limitation on reality. In other words, a scientist who makes the first move is
engaging in metaphysical disputation, while a scientist who makes the second is declining
to investigate a possible aspect of reality.
Unfortunately, many biologists make both moves, but fail to distinguish logically
between them. While justifying their exclusion of intelligent design on methodological
grounds, they act as though science has disproved its existence by providing a
naturalistic explanation for homology. When confronted with the fact that science has
failed in this regard, they reaffirm their methodological commitment and express faith
that a naturalistic mechanism will someday be discovered.
And perhaps it will. But what if living things really are designed? Someone who finds a
watch on the ground, and wants to investigate its origin, would be mistaken to rule out
design a priori. Having already jumped to the wrong conclusion, that person might
go on to waste an entire lifetime dabbling in spurious explanations. If science is
truth-seeking, then this is a strange way to do science.
According to an old joke, a passer-by walks up to a drunk stumbling around under a
street light. The passer-by asks the drunk what he's doing, and the drunk replies,
"Looking for my watch." "Oh, did you lose it here?" asks the
passer-by. "No," the drunk replies, "I lost it across the street, but
there's no light over there!" Letting naturalistic philosophical assumptions limit
one's search for the cause of homology may not be the best way to study living things.
Figure 4: Cleavage Stages
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Copyright © 1997 Jonathan Wells and Paul Nelson. All rights reserved.
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