ApostateAbe
Veteran Member
- Joined
- Sep 19, 2002
- Messages
- 1,299
- Location
- Colorado, USA
- Basic Beliefs
- Infotheist. I believe the gods to be mere information.
It follows from the fact that geneticists are always concerned with phenotypic differences that we need not be afraid of postulating genes with indefinitely complex phenotypic effects, and with phenotypic effects that show themselves only in highly complex developmental conditions. Together with Professor John Maynard Smith, I recently took part in a public debate with two radical critics of "sociobiology", before an audience of students. At one time in the discussion we were trying to establish that to talk of a gene "for X" is to make no outlandish claim, even where X is a complex, learned behaviour pattern. Maynard Smith reached for a hypothetical example and came up with a "gene for skill in tying shoelaces". Pandemonium broke loose at this rampant genetic determinism! The air was thick with the unmistakable sound of worst suspicions being gleefully confirmed. Delightedly sceptical cries drowned the quiet and patient explanation of just what a modest claim is being made whenever one postulates a gene for, say, skill in tying shoelaces. Let me explain the point with the aid of an even more radical-sounding yet truly innocuous thought experiment (Dawkins 1981).
Reading is a learned skill of prodigious complexity, but this provides no reason in itself for scepticism about the possible existence of a gene for reading. 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. In our educated environment it would properly be called a gene "for" dyslexia, since dyslexia would be its most salient consequence. Similarly, a gene which caused total blindness would also prevent reading, but it would not usefully be regarded as a gene for not reading. This is simply because preventing reading would not be its most obvious or debilitating phenotypic effect.
Returning to our gene for specific dyslexia, 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, because the logic of the terminology is identical in the two cases. 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 as to determine whether or not a person can learn to read, or how good he is at tying shoelaces, 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.
Reading is a learned skill of prodigious complexity, but this provides no reason in itself for scepticism about the possible existence of a gene for reading. 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. In our educated environment it would properly be called a gene "for" dyslexia, since dyslexia would be its most salient consequence. Similarly, a gene which caused total blindness would also prevent reading, but it would not usefully be regarded as a gene for not reading. This is simply because preventing reading would not be its most obvious or debilitating phenotypic effect.
Returning to our gene for specific dyslexia, 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, because the logic of the terminology is identical in the two cases. 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 as to determine whether or not a person can learn to read, or how good he is at tying shoelaces, 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.
~~Richard Dawkins, The Extended Phenotype: The Gene as the Unit of Selection, 1982, pages 22-23