The Extended Phenotype: The Long Reach of the Gene

by Richard Dawkins

Acknowledgements 1. Necker Cubes and Buffaloes 2. Genetic Determinism and Gene Selectionism 3. Constraints

packaged together in discrete ‘vehicles’ such as individual organisms, this is not fundamentally necessary. Rather, the replicator should be thought of as having extended phenotypic effects, consisting of all its effects on the world at large, not just its effects on the individual body in which it happens to be sitting.

‘What is its survival value?’ But we do not say, ‘What is the survival value of packaging life up into discrete units called organisms?’ We accept it as a given feature of the way life is. As

The purpose of this very simple model was to illustrate the kinds of conditions under which philandering might be favoured by natural selection, and the kinds of conditions under which faithfulness might be favoured. There was no presumption that philandering was more likely in males than faithfulness. Indeed, the particular run of the simulation that I published culminated in a mixed male population in which faithfulness slightly predominated (Dawkins 1976a, p. 165, although see Schuster & Sigmund 1981). There is not just one misunderstanding in Rose’s remarks, but multiple compounded misunderstanding. There is a wanton eagerness to misunderstand. It bears the stamp of snow-covered Russian jackboots, of little black microchips marching to usurp the male role and steal our tractor-drivers’ jobs. It is a manifestation of a powerful myth, in this case the great gene myth. The gene myth is epitomized in Rose’s parenthetic little joke about ladies not blaming their mates for sleeping around. It is the myth of ‘genetic determinism’. Evidently, for Rose, genetic determinism is determinism in the full philosophical sense of irreversible inevitability. He assumes that the existence of a gene ‘for’ X implies that X cannot be escaped. In the words of another critic of ‘genetic

We would also probably all three agree that human nervous systems are so complex that in practice we can forget about determinism and behave as if we had free will.

still a genetic difference. If it makes itself felt through some other medium, such that manipulations of the education system do not perturb it, it is, in principle, no more and no less a genetic difference than in the former, education-sensitive case: no doubt some other environmental manipulation could be found which did perturb it. Human psychological attributes vary along almost as many dimensions as psychologists can measure. It is difficult in practice (Kempthorne 1978), but in principle we could partition this variation among such putative causal factors as age, height, years of education, type of education classified in many different ways, number of siblings, birth order, colour of mother’s eyes, father’s skill in shoeing horses, and, of course, sex chromosomes. We could also examine two-way and multi-way interactions between such factors. For present purposes the important point is that the variance we seek to explain will have many causes, which interact in complex ways. Undoubtedly genetic variance is a significant cause of much phenotypic variance in observed populations, but its effects may be overridden, modified, enhanced, or reversed by other causes. Genes may modify the effects of other genes, and may modify the effects of the environment. Environmental events, both internal and external, may modify the effects of genes, and may modify the effects of other environmental events.

any suggestion that the child’s mathematical deficiency might have a genetic origin is likely to be greeted with something approaching despair: if it is in the genes ‘it is written’, it is ‘determined’ and nothing can be done about it; you might as well give up attempting to teach the child mathematics.

their effects than television, nuns, or

very much on how we are brought up, what diet or education we experience, and what other genes we happen to possess. So, of the two effects that genes have on the world—manufacturing copies of themselves, and influencing phenotypes—the first is inflexible apart from the rare possibility of mutation; the second may be exceedingly flexible. I think a confusion

‘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

environment. The reason why something so simple as a one

recombination data, where the genes for house colour sit on the chromosomes. This is, of course, hypothetical. I do not know of any genetic work on caddis houses, and it would be difficult

to breed in captivity (M. H. Hansell, personal communication). But my point is that, if the practical difficulties could be overcome, nobody would be very surprised if house colour did turn out to be a simple Mendelian character in accordance with my thought experiment. (Actually, colour is a slightly unfortunate example to have chosen, since caddis vision is poor and they almost certainly ignore visual cues in choosing stones. Rather than use a more realistic example like stone shape (Hansell), I stay with colour for the sake of the analogy with the black pigment discussed above.) The interesting sequel is this. House colour is determined by the colour of the stones chosen from the stream bed by the larva, not by the biochemical synthesis of a black pigment. The genes determining house colour must work via the behavioural mechanism that chooses stones, perhaps via the eyes. So much would be agreed by any ethologist. All that this chapter adds is a logical point: once we have accepted that there are genes for building behaviour, the rules of existing terminology imply that the artefact itself should be treated as part of the phenotypic expression of genes in the animal. The stones are outside the body of the organism, yet logically such a gene is a gene ‘for’ house colour, in exactly as strong a sense as the hypothetical gene B was for skin colour. And B was indeed a gene for skin colour, even though

bank within a reasonable distance. By building a dam across the

has done a genetic study of beaver dams, but we

of beaver genes. It is enough that we accept that beaver dams must have evolved by Darwinian natural selection: this can only have come about if dams have varied under the control of genes (Chapter 2). Just by talking about a few examples of animal artefacts, then, we have pushed the conceptual range of the gene’s phenotype

make of an artefact that is the joint production of a pair of animals

nest. This, however, is only a relative complication. Fundamentally what is going on is that genes, compared with their alleles, exert quantitative, mutually interacting, mutually modifying, effects on a shared phenotype, the mound. They do this proximally by controlling the chemistry of cells in worker bodies, and hence worker behaviour. The principle is the same, whether the cells happen to