The Information - James Gleick [147]
So geneticists and zoologists and ethologists and paleontologists all got into the habit of saying “a gene for X” instead of “a genetic contribution to the variation in X.”♦ Dawkins was forcing them to face the logical consequences. If there is any genetic variation in a trait—eye color or obesity—then there must be a gene or genes for that trait. It doesn’t matter that the actual appearance of the trait may depend on an unfathomable array of other factors, which may be environmental or even accidental. By way of illustration, he offered a deliberately extreme example: a gene for reading.
The idea seems absurd, for several reasons. Reading is learned behavior. No one is born able to read. If ever a skill depends on environmental factors, such as education, it is reading. Until a few millennia ago, the behavior did not exist, so it could not have been subject to natural selection. You might as well say (as the geneticist John Maynard Smith did, mockingly) that there is a gene for tying shoelaces. But Dawkins was undaunted. He pointed out that genes are about differences, after all. So he began with a simple counterpoint: might there not be a gene for dyslexia?
All we would need in order to establish the existence of a gene for reading is to discover a gene for not reading, say a gene which induced a brain lesion causing specific dyslexia. Such a dyslexic person might be normal and intelligent in all respects except that he could not read. No geneticist would be particularly surprised if this type of dyslexia turned out to breed true in some Mendelian fashion. Obviously, in this event the gene would only exhibit its effect in an environment which included normal education. In a prehistoric environment it might have had no detectable effect, or it might have had some different effect and have been known to cave-dwelling geneticists as, say, a gene for inability to read animal footprints.…
It follows from the ordinary conventions of genetic terminology that the wild-type gene at the same locus, the gene that the rest of the population has in double dose, would properly be called a gene “for reading.” If you object to that, you must also object to our speaking of a gene for tallness in Mendel’s peas.… In both cases the character of interest is a difference, and in both cases the difference only shows itself in some specified environment. The reason why something so simple as a one gene difference can have such a complex effect … is basically as follows. However complex a given state of the world may be, the difference between that state of the world and some alternative state of the world may be caused by something extremely simple.♦
Can there be a gene for altruism? Yes, says Dawkins, if this means “any gene that influences the development of nervous systems in such a way as to make them likely to behave altruistically.”♦ Such genes—these replicators, these survivors—know nothing about altruism and nothing about reading, of course. Whatever and wherever they are, their phenotypic effects matter only insofar as they help the genes propagate.
Molecular biology, in its signal achievement, had pinpointed the gene in a protein-encoding piece of DNA. This was the hardware definition. The software definition was older and fuzzier: the unit of heredity; the bearer of a phenotypic difference. With the two definitions uneasily coexisting, Dawkins looked past them both.
If genes are meant to be masters of survival, they can hardly be fragments of nucleic acid. Such things are fleeting. To say that a replicator manages to survive for eons is to define the replicator as all the copies considered as one. Thus the gene does not “grow senile,” Dawkins declared.
It is no more likely to die when it is a million years old than when it is only a hundred. It leaps from body to body down the generations, manipulating body after body in its own way and for its own ends,