efore Darwin, homology was defined morphologically and
explained by reference to ideal archetypes, - that is, to supernatural
design. Darwin reformulated biology in naturalistic* rather than idealistic
terms, and explained homology as the result of descent with modification
from a common ancestor. Descent with modification, however, renders design
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
*[In this paper, “naturalism” and “naturalistic” refer to the
philosophical doctrine that nature is the whole of reality, and that ideas
and supernatural entities are human projections.]
Morphological and Phylogenetic 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
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
conform 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 supernatural agency) 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)
The concept of homology can thus function in several ways, which can be
brought into sharper focus by placing them in the context of syllogisms:
A. Classical (morphological) view:
Premise 1 (Definition). Features are homologous if and only if they have similar structures.
Premise 2 (Empirical observation). A bat’s wing and a whale’s
flipper have similar structures.
Conclusion. Therefore, a bat’s wing and a whale’s flipper are
A'. Darwin’s extension of the morphological view:
Premise 1 (Conclusion from classical view). A bat’s wing and a
whale’s flipper are homologous features.
Premise 2 (Proposed explanation). Features are homologous because they are inherited from a common ancestor.
Conclusion. Therefore, a bat’s wing and a whale’s flipper are
inherited from a common ancestor.
B. Post-Darwinian (phylogenetic) view:
Premise 1 (Definition). Features are homologous if and only if
they are inherited from a common ancestor.
Premise 2 (Assumption? Empirical inference?). A bat’s wing and a whale’s flipper are inherited from a common ancestor.
Conclusion. Therefore, a bat’s wing and a whale’s flipper are
Ironically, the post-Darwinian (phylogenetic) definition of homology
undercuts one of Darwin’s own arguments for evolution, since it requires
that common ancestry be established (or assumed) before features can be
called homologous. Logically speaking, it is a fallacy to infer evolution
from phylogenetic homology: once one determines (or assumes) that features
are homologous because of common ancestry, it would be circular reasoning
to claim that homology demonstrates common ancestry. This does not mean,
however, that structural similarities can no longer be used to infer
homology, but only that they must be traced back through a fossil lineage
to a common ancestor. For example, the similar bone structures in a bat’s
wing and a whale’s flipper cannot, by themselves, justify an inference of
phylogenetic homology. But if one could establish that fossil bats and
fossil whales are more similar in this regard than extant organisms, -
especially if the fossils suggest gradual divergence from a presumed common
ancestor, - then one could infer that they are phylogenetically homologous.
The Need For A Naturalistic Mechanism
It turns out, however, that tracing structural similarities back through
fossils to a presumed common ancestor is insufficient to exclude archetypes
or design-based explanations. 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; emphasis in the original) 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 Supernatural 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 preexisting
patterns, i.e., to design. Ironically, therefore, Berra’s analogy shows
that phylogenetic homology is 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
move may seem very reasonable, however, it 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 discipline, not
a description of objective reality. If evolutionary biologists want to show
that the actual mechanism of evolution does not involve Supernatural
design, they cannot merely exclude the possibility a priori, but must take
the more difficult approach of proposing and corroborating a naturalistic
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
Homology And Genetics
One possibility is that this information is encoded in the organism’s
genes. In the 1930s, 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”). 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 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 involve 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) In 1985, 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 [emphasis added]) 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
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
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 dissimilar
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
from distinctly dissimilar initial states.” (Alberch, 1985, p. 51 [emphasis added])
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
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. (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 [emphasis added])
The constancy of final patterns despite varying pathways has prompted
developmental biologist Gunter 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
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 [emphasis added]) 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 natural.
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 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 [emphasis added]) Twenty-five
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 idealized 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 supernatural design does
not exist, or it could be taken as a statement that supernatural design is
beyond the reach of empirical science. The first is a theological
statement, and warrants a theological 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 theological 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 supernatural
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
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
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.
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