I first heard this argument in a public debate with Drs. Gish and Parker of the Institute for Creation Research (7 November 1979). The creationist presentation goes something like this:
Evolutionists claim that homologous structures, for example the wing of a bird and the forelimb of a reptile, evolved from an ancestral leg. If this is fact, then the genes for reptile legs and bird wings should also be homologous or similar. But the evolutionist finds himself in big trouble with this assumption because the world-famous evolutionist, Sir Gavin de Beer, presents evidence that the genes can change completely without the organ determined by the genes changing at all. In fact de Beer concludes and I quote: "It is now clear that the pride with which it was assumed that the inheritance of homologous structures from a common ancestor explained homology was misplaced. For such inheritance can not be ascribed to identity of genes. The attempt to find homologous genes except in closely related species has been given up as hopeless."
At first glance this seems like a rather exciting observation. If the genes for homologous structures are not themselves homologous, then our understanding of evolution would have to undergo some major revisions. If true, it would mean that the "evolutionary" sequences found in the fossil record cannot be explained by any systematic genetic changes. However, once our excitement wears off, we begin to ask how this most interesting of genetic observations was made. After all I was not aware that anyone had yet been so clever as to identify a gene which is directly responsible for the normal shape of some structure such as a wing. We have, of course, studied many genes in the fruit fly which cause abnormal development of a wing or an eye, but that does not allow us to conclude that these mutations are alterations of the very genes which control the normal structure. These mutant genes affecting structure may act by circuitous routes.
Even when we eventually do identify genes which are directly responsible for controlling normal structures, it will be quite a problem to isolate these genes so that we can determine their molecular structure, the DNA code sequence. I can assure the reader that such developments are at least several years down the road. So how in heaven's name did de Beer reach his startling conclusion? To begin with I found that our library didn't have the de Beer reference Dr. Gish had quoted, so Dr. Gish kindly loaned me his copy. The reference turned out to be one of a collection of "Oxford Biology Readers" written for high school students. Thus, it is neither a research paper nor a scholarly monograph. The particular reader to which Dr. Gish referred is titled "Homology, An Unsolved Problem" (published by Oxford University Press, 1971) and the above quote is found on page 16.
De Beer's conclusion is based on genetic experiments with fruit flies. He notes that a pure-breeding line of flies without eyes has been established by genetic investigators. From time to time this line produces an occasional fly which has eyes. When such a normal-looking fly mates with a standard fly, they can produce eyeless offspring. So the normal-looking parent apparently still had the genes for the missing eyes. Then it holds, de Beer goes on to say, that the normal-looking parent fly enjoyed the use of his eyes because other genes took the place of the missing eye genes. De Beer asks why other genes should know how to stand in for the original eye gene. And he concludes that "Homologous structures need not be controlled by identical genes, and homology of phenotypes does not imply similarity of geneotypes." In other words, similar structures do not imply similar genes. This astonishing conclusion, if substantiated, thoroughly undermines modern evolution theory.
A contemporary geneticist, however, has no difficulty in proposing a viable explanation for this experiment. The occasional normal-looking flies probably were produced from the eyeless line through the action of "suppressor" mutations, i.e., additional mutations which restore the normal appearance of a mutant organism.
Countless investigations done in the last quarter of a century have shown similar cases of mutant gene suppression in a wide variety of organisms. Suppressors have been shown to act by means of a variety of mechanisms, but virtually none, if any, acts by replacing the function of the original "missing gene." In fact many studies have shown that the original "missing gene" is usually not missing at all, but is merely altered in some minor way so that it can no longer function normally. The only thing that suppressors have in common is that each is a second mutation which is able to negate the mutant expression of the original mutant gene that it suppresses. Perhaps the original eyeless gene causes the production of an incorrect initiator of eye structure, and the suppressor gene makes abnormal cells which can now respond correctly to the incorrect initiation signal. In a sense this is a case of two wrongs making a right.
Surely de Beer could have thought of this or some other non-paradoxical explanation. Perhaps his purpose in the Oxford Reader Series was to stimulate the thinking of his student readers. He may have assumed that his readers would not yet know about suppressor genes, and that the pedagogical value of presenting an apparent paradox would outweigh whatever worth there might be in an attempt to provide an up-to-the-minute answer for every question. Apparently Dr. Gish has never heard of suppressor genes. So instead of trying to resolve de Beer's paradox in terms of modern research, he preferred to use what may be a teaching tactic as the last word on the subject.