The Extended Phenotype: The Long Reach of the Gene

by Richard Dawkins

either his polyandrous tribes had to have been living, in partial genetic isolation, under their peculiar conditions for a large number of centuries, or natural selection had to have favoured the universal occurrence of genes programming some complex ‘conditional strategy’.

It may be that the phenotype which we are trying to explain did not even exist in some earlier environment, even though the gene did then exist.

In this example the angler wins the arms race against its prey, simply because its side of the arms race constitutes a relatively negligible threat to any given individual of the other side, through being rare.

Do not expect to see animals always behaving in such a way as to maximize their own inclusive fitness. Losers in an arms race may behave in some very odd ways indeed. If they appear disoriented and unsure of their footing, this may be only the beginning.

If M. santschii is sufficiently rare, it is easy to see that it might ‘win’ the arms race, even though regicide is such a disastrous act for each host colony whose workers succumb to it.

Therefore if there is any question of manipulation in this situation, parental manipulation of offspring is more likely than offspring manipulation of parents.

but because the genes that exist today are a selected set, and the qualities that made them survive reflect the qualities of the environments in which they survived. I said that a gene’s experience consists

Just as too small a parliament may be perverted by the Cabals of a few, a species with only one, slightly linked chromosome is an easy prey to distorters’

‘approximately half the genome is maintained as a linkage group with the sex chromosome’

a high chromosome number in a species tends to go with low genetic variance among siblings in that species.

The hypothesis may be rescued from this objection by suggesting that high chromosome numbers are not an adaptation to facilitate queen manipulation of workers, but rather are a preadaptation. Those groups that happened, for other reasons, to have high chromosome numbers were the most likely to evolve eusociality.

In bacteria, recombination is achieved by a separate fragment of DNA or ‘sex factor’ which, in older textbooks, was treated as a part of the bacterium’s own adaptive machinery, but which is better regarded as a replicating genetic engineer working for its own good.

DNA is not working for the good of the cell but for the good of itself.

saw the utility of within-body selection as a solution to the coadaptation problem.

depends upon our definition of the germ-line.

If it is measured as number of offspring reaching reproductive age it neglects variation in reproductive success of the grown offspring. If it is measured as number of grandchildren it neglects . . . and so on ad infinitum.

If we look far enough into the future, either I shall have no descendants at all, or all persons alive will be my descendants

Inclusive fitness is calculated from an individual’s own reproductive success plus his effects on the reproductive success of his relatives, each one weighed by the appropriate coefficient of relatedness.

We could compare the effects of his choosing to perform act X rather than act Y.

Environment’, in that last clause, is taken to include all the genes at other loci that must be present in order for P1 or P2 to be expressed.

unless some of the variation in the population is due to lack of A. If

The principle is the same, whether the cells happen to be organized into one large homogeneous clone, as in the human body, or into a heterogeneous collection of clones, as in the termite mound.

This means that the workers building the later parts of a mound may not be full siblings of those that began the task, but their nephews and nieces (probably inbred and rather uniform, incidentally—Hamilton 1972; Bartz 1979). These later reproductives still draw their genes from the ‘tetraploid’ set introduced by the original royal pair, but their progeny will permute a particular subset of those original genes.

might expect that disputes resulting from genetic heterogeneity in termites would be resolved by similar rules. In this way the extended phenotype could take up a discrete and regular shape, despite being built by genetically heterogeneous workers.

The proximal phenotypic power of the symbiont genes is exerted via protein synthesis in symbiont cytoplasm. But just as termite genes reach out beyond the cells that enclose them and manipulate the development of whole termite bodies and hence of the mound, is it not almost inevitable that the symbiont genes will have been selected to exert phenotypic power on their surroundings?

devoid of discussion on why they might have been selected to do so, or whether, instead, castration is simply a fortuitous byproduct of parasitization.

and so might bacterial endosymbionts of insects which are transmitted transovarially and in some cases seem to influence the host sex ratio

because their destiny is shared for only a short part of the future: their common cause is limited to the life of the present host body, and does not carry over into the gametes and offspring of the present host.

A gene, whether a host gene or a parasite gene, can exert a more fundamental influence on the final host phenotype if it acts early in the development of the host embryo than if it acts late.

Genes in male mice have phenotypic expression in female bodies, in just the same sense as genes in mother snails have phenotypic expression in the bodies of their children.

Human red blood cells, for instance, have no nuclei, and must express the phenotypes of genes in other cells. So why should we not, when the occasion warrants it, conceive of the bridging of gaps between cells in different bodies?

the consequences of the gene’s action to feed back and affect the welfare of the gene itself.

An animal’s behaviour tends to maximize the survival of the genes ‘for’ that behaviour,

Adaptations benefit the genetic replicators responsible for them, and only incidentally the individual organisms involved.

generations as all directed towards the final end of sexual reproduction in autumn. Asexual reproduction, according to this view, is not really reproduction at all. It is growth, just like the growth of a single elephant’s body.

equate the reproduction/growth distinction with the sexual/asexual distinction.

Is there really a crucial difference between ‘reproducing’ to make two aphids on the one hand, and ‘growing’ to make one aphid twice as large on the other? Janzen

that a lineage of R is capable of evolving complex adaptations in a way that G is not. The reasoning goes as follows.

But the evolution of organs and adaptations at the multicellular level could not take place, because recurrent, cyclical development of whole groups of cells does not occur.

rest. In order to put together new complexity, new developmental beginnings are required.

An organism is the physical unit associated with one single life cycle.

but this leads to evolutionary change only if the replicators are in germ-lines. A

Therefore we may still talk meaningfully about vehicle selection between plants in a population of plants, but the inter-plant selection pressure may have to be strong to outweigh selection among cells within plants. This is, incidentally, analogous to one of the conditions for ‘kin-group selection’ (Hamilton 1975a) to work. To make the analogy, we have only to see the plant as a ‘group’ of cells.

other: they are descended from a single stem cell, which means that they have a more recent common ancestor with each other than with the cells of any other organism.