The Extended Phenotype Quotes

In the world of the extended phenotype, ask not how an animal's behaviour benefits its genes; ask instead whose genes it is benefiting.

Putting these three things together we arrive at our own ‘central theorem’ of the extended phenotype: An animal’s behaviour tends to maximize the survival of the genes ‘for’ that behaviour, whether or not those genes happen to be in the body of the particular animal performing it.

With only a little imagination we can see the gene as sitting at the centre of a radiating web of extended phenotypic power.

This 'web of discourses' as Robyn called it...is as much a biological product as any of the other constructions to be found in the animal world. (Clothes too, are part of the extended phenotype of Homo Sapiens almost every niche inhabited by that species.An illustrated encyclopedia of zoology should no more picture Homo Sapiens naked than it should picture Ursus arctus-the black bear- wearing a clown suit and riding a bicycle.

Genes affect proteins, and proteins affect X which affects Y which affects Z which . . . affects the phenotypic character of interest.

A replicator may be said to ‘benefit’ from anything that increases the number of its descendant (‘germ-line’) copies.

The genes in one organism’s cells, then, can have extended phenotypic influence on the living body of another organism; in this case a parasite’s genes find phenotypic expression in the behaviour of its host.

An organism is the physical unit associated with one single life cycle. Replicators that gang up in multicellular organisms achieve a regularly recycling life history, and complex adaptations to aid their preservation, as they progress through evolutionary time.

Of course genes are not directly visible to selection. Obviously they are selected by virtue of their phenotypic effects, and certainly they can only be said to have phenotypic effects in concert with hundreds of other genes. But it is the thesis of this book that we should not be trapped into assuming that those phenotypic effects are best regarded as being neatly wrapped up in discrete bodies (or other discrete vehicles). The doctrine of the extended phenotype is that the phenotypic effect of a gene (genetic replicator) is best seen as an effect upon the world at large, and only incidentally upon the individual organism—or any other vehicle—in which it happens to sit.

Natural selection favours those genes that manipulate the world to ensure their own propagation. This leads to what I have called the central theorem of the extended phenotype: An animal’s behaviour tends to maximize the survival of the genes ‘for’ that behaviour, whether or not those genes happen to be in the body of the particular animal performing it.

Why are genetic determinants thought to be any more ineluctable, or blame-absolving, than ‘environmental’ ones?

The whole purpose of our search for a ‘unit of selection’ is to discover a suitable actor to play the leading role in our metaphors of purpose.

The controversy about group selection versus individual selection is a controversy about the rival claims of two suggested kinds of vehicle.

I define a replicator as anything in the universe of which copies are made.

Replicators may be classified in two ways. They may be ‘active’ or ‘passive’, and, cutting across this classification, they may be ‘germ-line’ or ‘dead-end’ replicators.

In principle, we may consider any portion of chromosome as a potential candidate for the title of replicator.

Germ-line replicators, then, are units that actually survive or fail to survive, the difference constituting natural selection.

Active replicators have some effect on the world, which influences their chances of surviving.

It is the effects on the world of successful active germ-line replicators that we see as adaptations.

Any effect that a meme has on the behaviour of a body bearing it may influence that meme’s chance of surviving.

Finally, at the end of the chapter, we saw that genes ‘sharing’ a given extended phenotypic trait might come from different species, even different phyla and different kingdoms.

One is that phenotypes that extend outside the body do not have to be inanimate artefacts: they can themselves be built of living tissue.

The other idea is that wherever there are ‘shared’ genetic influences on an extended phenotype, the shared influences may be in conflict with each other rather than cooperative

The second point of this present chapter is that the genes that bear upon any given extended phenotypic trait may be in conflict rather than in concert with one another.

A further important point is that Maynard Smith was seeking the ‘best’ strategy in only a special sense. In fact he was seeking an ‘evolutionarily stable strategy’ or ESS.

The ESS has been rigorously defined (Maynard Smith 1974), but it can be crudely encapsulated as a strategy that is successful when competing with copies of itself.

A passive replicator is a replicator whose nature has no influence over its probability of being copied.

But whether it succeeds in practice or not, any germ-line replicator is potentially immortal. It ‘aspires’ to immortality but in practice is in danger of failing.

As I said, the active/passive distinction cuts across the germ-line/dead-end distinction. All four combinations are conceivable.

Particular interest attaches to one of the four, the active germ-line replicator, for it is, I suggest, the ‘optimon’, the unit for whose benefit adaptations exist.

To the extent that active germ-line replicators benefit from the survival of bodies other than those in which they sit, we may expect to see ‘altruism’, parental care, etc.

The word replicator is purposely defined in a general way, so that it does not even have to refer to DNA.

I am, indeed, quite sympathetic towards the idea that human culture provides a new milieu in which an entirely different kind of replicator selection can go on.

Natural selection may usually be safely regarded as the differential survival of replicators relative to their alleles.

The word allele is nowadays customarily used of cistrons but it is clearly easy, and in the spirit of this chapter, to generalize it to any portion of chromosome.

An arbitrarily defined length of chromosome, or potential replicator, may be said to have an expected half-life, measured in generations.

It is widely admitted that serious error follows from the uncritical assumption that adaptations are for the good of the species.

They are the outward and visible (audible, etc.) manifestations of the memes within the brain.

The new copy of the meme is then in a position to broadcast its phenotypic effects, with the result that further copies of itself may be made in yet other brains.

The point is the obvious one that selection at any one locus is not independent of selection at other loci.

Whatever the claims of memes to be regarded as replicators in the same sense as genes, the first part of this chapter established that individual organisms are not replicators.

Nevertheless, they are obviously functional units of great importance, and it is now necessary to establish exactly what their role is.

There is a hierarchy of entities embedded in larger entities, and in theory the concept of vehicle might be applied to any level of the hierarchy.

Functionally speaking, too, genes are gregarious. They have phenotypic effects on bodies, but they do not do so in isolation. I stress this over and over again in this book.

Selection favours those genes which succeed in the presence of other genes, which in turn succeed in the presence of them.

To the extent that active germ-line replicators benefit from the survival of the bodies in which they sit, we may expect to see adaptations that can be interpreted as for bodily survival.

The point about recurrent reproduction life cycles, and hence, by implication, the point about organisms, is that they allow repeated returns to the drawing board during evolutionary time.

What does complementariness mean for genes? Two genes may be said to be complementary if the survival of each, relative to its alleles, is enhanced when the other is abundant in the population.

Most of the DNA molecules in our bodies are dead-end replicators. They may be the ancestors of a few dozen generations of mitotic replication, but they will definitely not be long-term ancestors.

To regard an organism as a replicator, even an asexual organism like a female stick insect, is tantamount to a violation of the ‘central dogma’ of the non-inheritance of acquired characteristics.

The controversy about gene selection versus individual (or group) selection is a controversy about whether, when we talk about a unit of selection, we ought to mean a vehicle at all, or a replicator.

the conclusion I wish to draw is not really disputable. If host behaviour or physiology is a parasite adaptation, there must be (have been) parasite genes ‘for’ modifying the host, and the host modifications are therefore part of the phenotypic expression of those parasite genes. The extended phenotype reaches out of the body in whose cells the genes lie, reaches out to the living tissues of other organisms.

the behaviour of an individual may not always be interpretable as designed to maximize its own genetic welfare: it may be maximizing somebody else’s genetic welfare, in this case that of a parasite inside it.

If two beavers working on the same dam have different genes for dam height, the resulting extended phenotype will reflect the interaction between the genes, in the same way as bodies reflect gene interactions.

I have previously supported the case for a completely non-genetic kind of replicator, which flourishes only in the environment provided by complex, communicating brains. I called it the ‘meme’ (Dawkins 1976a).

The phenotypic effects of a meme may be in the form of words, music, visual images, styles of clothes, facial or hand gestures, skills such as opening milk bottles in tits, or panning wheat in Japanese macaques.

This, then, is our candidate replicator. But a candidate should be regarded as an actual replicator only if it possesses some minimum degree of longevity/fecundity/fidelity (there may be trade-offs among the three).

If the parasite’s means of genetic exit from the host’s body is the same as the host’s, namely the host’s gametes or spores, there will be relatively little conflict between the ‘interests’ of parasite and host genes.

Adoption and contraception, like reading, mathematics, and stress-induced illness, are products of an animal that is living in an environment radically different from the one in which its genes were naturally selected.

Phenotypic effects of genes, whether at the level of intracellular biochemistry, gross bodily morphology, or extended phenotype, are potentially devices by which genes lever themselves into the next generation, or barriers to their doing so. Incidental side-effects are not always effective as tools or barriers, and we do not bother to regard them as phenotypic expressions of genes, either at the conventional or the extended phenotype level.

Just as every gene is the centre of a radiating field of influence on the world, so every phenotypic character is the centre of converging influences from many genes, both within and outside the body of the individual organism.

If the phenotypic change in the artefact had an influence on the success of replication of the new gene, natural selection would act, positively or negatively, to change the probability of similar artefacts existing in the future.

They may be perceived by the sense organs of other individuals, and they may so imprint themselves on the brains of the receiving individuals that a copy (not necessarily exact) of the original meme is graven in the receiving brain.

To the extent that active germ-line replicators benefit from the survival of the group of individuals in which they sit, over and above the two effects just mentioned, we may expect to see adaptations for the preservation of the group.

Most of the replicators in the world have won their place in it by defeating all available alternative alleles. The weapons with which they won, and the weapons with which their rivals lost, are their respective phenotypic consequences

It is fundamental to the idea of a replicator that when a mistake or ‘mutation’ does occur it is passed on to future copies: the mutation brings into existence a new kind of replicator which ‘breeds true’ until there is a further mutation

From the viewpoint of this book an animal artefact, like any other phenotypic product whose variation is influenced by a gene, can be regarded as a phenotypic tool by which that gene could potentially lever itself into the next generation.

It is, of course, true that ‘Memes are utterly dependent upon genes, but genes can exist and change quite independently of memes’ (Bonner 1980). But this does not mean that the ultimate criterion for success in meme selection is gene survival.

It is these phenotypic effects that we see as adaptations to survival. When we ask whose survival they are adapted to ensure, the fundamental answer has to be not the group, nor the individual organism, but the relevant replicators themselves.

The gene’s extended phenotypic effect, say an increase in the height of the dam, affects its chances of survival in precisely the same sense as in the case of a gene with a normal phenotypic effect, such as an increase in the length of the tail.

Replicator selection is the process by which some replicators survive at the expense of other replicators. Vehicle selection is the process by which some vehicles are more successful than other vehicles in ensuring the survival of their replicators

We have now also seen that, in precisely the same sense as it is ever possible to talk of a gene ‘for’ a behaviour pattern, it is possible to talk of a gene, in one organism, ‘for’ a behaviour pattern (or other phenotypic characteristic) in another organism.

A dead-end replicator (which also may be active or passive) is a replicator which may be copied a finite number of times, giving rise to a short chain of descendants, but which is definitely not the potential ancestor of an indefinitely long line of descendants.

If replicators exist that are active, variants of them with certain phenotypic effects tend to out-replicate those with other phenotypic effects. If they are also germ-line replicators, these changes in relative frequency can have long-term, evolutionary impact.

An extended phenotypic character is the product of the interaction of many genes whose influence impinges from both inside and outside the organism. The interaction is not necessarily harmonious—but then nor are gene interactions within bodies necessarily harmonious,

An active replicator is any replicator whose nature has some influence over its probability of being copied. For example a DNA molecule, via protein synthesis, exerts phenotypic effects which influence whether it is copied: this is what natural selection is all about.

Evolution is the external and visible manifestation of the differential survival of alternative replicators (Dawkins 1978a). Genes are replicators; organisms and groups of organisms are best not regarded as replicators; they are vehicles in which replicators travel about.

To recapitulate, the significance of the difference between growth and reproduction is that reproduction permits a new beginning, a new developmental cycle, and a new organism which may be an improvement, in terms of the fundamental organization of complex structure, over its predecessor.

Each gene works in a world of phenotypic consequences of other genes. Some of those other genes will be members of the same genome. Others will be members of the same gene-pool operating through other bodies. Yet others may be members of different gene-pools, different species, different phyla.

It seems to follow from the thesis of this book that there is no important distinction between our ‘own’ genes and parasitic or symbiotic insertion sequences. Whether they conflict or cooperate will depend not on their historical origins but on the circumstances from which they stand to gain now.

A germ-line replicator (which may be active or passive) is a replicator that is potentially the ancestor of an indefinitely long line of descendant replicators. A gene in a gamete is a germ-line replicator. So is a gene in one of the germ-line cells of a body, a direct mitotic ancestor of a gamete.

Returning, for clarification, to DNA as our archetypal replicator, its consequences on the world are of two important types. Firstly, it makes copies of itself, making use of the cellular apparatus of replicases, etc. Secondly, it has effects on the outside world, which influence the chances of its copies’ surviving.

When we talk of a program as ‘doing better’ or as being ‘successful’ we are notionally measuring success as capacity to propagate copies of the same program in the next generation: in reality this is likely to mean that a successful program is one which promotes the survival and reproduction of the animal adopting it.

If the organism is not a replicator, what is it? The answer is that it is a communal vehicle for replicators. A vehicle is an entity in which replicators (genes and memes) travel about, an entity whose attributes are affected by the replicators inside it, an entity which may be seen as a compound tool of replicator propagation.

It will be remembered that the ‘central theorem’ of the selfish organism claims that an animal’s behaviour tends to maximize its own (inclusive) fitness. We saw that to talk of an individual behaving so as to maximize its inclusive fitness is equivalent to talking of the gene or genes ‘for’ that behaviour pattern maximizing their survival.

Replicators need not last forever. They need only last long enough to produce additional replicators [fecundity] that retain their structure largely intact [fidelity]. The relevant longevity concerns the retention of structure through descent. Some entities, though structurally similar, are not copies because they are not related by descent.

Two kinds of factor will affect this half-life. Firstly, replicators whose phenotypic effects render them successful at their business of propagating themselves will tend to have a long half-life. Replicators with longer half-lives than their alleles will come to predominate in the population, and this is the familiar process of natural selection.

A DNA molecule in the germ-line of an individual who happens to die young, or who otherwise fails to reproduce, should not be called a dead-end replicator. Such germ-lines are, as it turns out, terminal. They fail in what may metaphorically be called their aspiration to immortality. Differential failure of this kind is what we mean by natural selection.

The integrated multicellular organism is a phenomenon which has emerged as a result of natural selection on primitively independent selfish replicators. It has paid replicators to behave gregariously. The phenotypic power by which they ensure their survival is in principle extended and unbounded. In practice the organism has arisen as a partially bounded local concentration, a shared knot of replicator power.

Natural selection is the process whereby replicators out-propagate each other. They do this by exerting phenotypic effects on the world, and it is often convenient to see those phenotypic effects as grouped together in discrete ‘vehicles’ such as individual organisms. This gives substance to the orthodox doctrine that each individual body can be thought of as a unitary agent maximizing one quantity—‘fitness’,

We are fundamentally interested in natural selection, therefore in the differential survival of replicating entities such as genes. Genes are favoured or disfavoured relative to their alleles as a consequence of their phenotypic effects upon the world. Some of these phenotypic effects may be incidental consequences of others, and have no bearing on the survival chances, one way or the other, of the genes concerned.

The genotype may be a ‘physiological team’, but we do not have to believe that that team was necessarily selected as a harmonious unit in comparison with less harmonious rival units. Rather, each gene was selected because it prospered in its environment, and its environment necessarily included the other genes which were simultaneously prospering in the gene-pool. Genes with complementary ‘skills’ prosper in each others’ presence.

If a program or strategy is successful, this means that copies of it will tend to become more numerous in the population of programs and will ultimately become almost universal. It will therefore come to be surrounded by copies of itself. If it is to remain universal, therefore, it must be successful when competing against copies of itself, successful compared with rare different strategies that might arise by mutation or invasion.

A stick insect looks like a replicator, in that we may lay out a sequence consisting of daughter, granddaughter, great-granddaughter, etc., in which each appears to be a replica of the preceding one in the series. But suppose a flaw or blemish appears somewhere in the chain, say a stick insect is unfortunate enough to lose a leg. The blemish may last for the whole of her lifetime, but it is not passed on to the next link in the chain.

But if we set selection pressures on one side, we can say something about the half-life of a replicator on the basis of its length alone. If the stretch of chromosome we choose to define as our replicator of interest is long, it will tend to have a shorter half-life than a shorter replicator, simply because it is more likely to be broken by crossing-over. A very long portion of chromosome ceases to deserve the title of replicator at all.

The facts are as follows. The total amount of DNA in different organisms is very variable, and the variation does not make obvious sense in terms of phylogeny. This is the so-called ‘C-value paradox’. ‘It seems totally implausible that the number of radically different genes needed in a salamander is 20 times that found in a man’ (Orgel & Crick 1980). It is equally implausible that salamanders on the West side of North America should need many times more DNA than congeneric salamanders on the East side.

My thesis has been that the slight further conceptual step outside the immediate body is a comparatively minor one. Nevertheless it is an unfamiliar one, and I tried to develop the idea in stages, working through inanimate artefacts to internal parasites controlling their hosts’ behaviour. From internal parasites we moved via cuckoos to action at a distance. In theory, genetic action at a distance could include almost all interactions between individuals of the same or different species. The living world can be seen as a network of interlocking fields of replicator power.

These phenotypic consequences are conventionally thought of as being restricted to a small field around the replicator itself, its boundaries being defined by the body wall of the individual organism in whose cells the replicator sits. But the nature of the causal influence of gene on phenotype is such that it makes no sense to think of the field of influence as being limited in this arbitrary way, any more than it makes sense to think of it as limited to intracellular biochemistry. We must think of each replicator as the centre of a field of influence on the world at large.

But there is nothing magic about Darwinian fitness in the genetic sense. There is no law giving it priority as the fundamental quantity that is maximized. Fitness is just a way of talking about the survival of replicators, in this case genetic replicators. If another kind of entity arises, which answers to the definition of an active germ-line replicator, variants of the new replicator that work for their own survival will tend to become more numerous. To be consistent, we could invent a new kind of ‘individual fitness’, which measured the success of an individual in propagating his memes.

To the extent that active germ-line replicators benefit from the survival of the bodies in which they sit, we may expect to see adaptations that can be interpreted as for bodily survival. A large number of adaptations are of this type. To the extent that active germ-line replicators benefit from the survival of bodies other than those in which they sit, we may expect to see ‘altruism’, parental care, etc. To the extent that active germ-line replicators benefit from the survival of the group of individuals in which they sit, over and above the two effects just mentioned, we may expect to see adaptations for the preservation of the group.