The Extended Phenotype - The Long Reach of the Gene

The thesis that I shall support is this. It is legitimate to speak of adaptations as being ‘for the benefit of’ something, but that something is best not seen as the individual organism. It is a smaller unit which I call the active, germ-line replicator. The most important kind of replicator is the ‘gene’ or small genetic fragment.

Replicators are not, of course, selected directly, but by proxy; they are judged by their phenotypic effects.

If society systematically trains children without penises to knit and play with dolls, and trains children with penises to play with guns and toy soldiers, any resulting differences in male and female preferences are strictly speaking genetically determined differences! They are determined, through the medium of societal custom, by the fact of possession or non-possession of a penis, and that is determined (in a normal environment and in the absence of ingenious plastic surgery or hormone therapy) by sex chromosomes.

If a child has had bad teaching in mathematics, it is accepted that the resulting deficiency can be remedied by extra good teaching the following year. But 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. This is pernicious rubbish on an almost astrological scale. Genetic causes and environmental causes are in principle no different from each other. Some influences of both types may be hard to reverse; others may be easy to reverse. Some may be usually hard to reverse but easy if the right agent is applied. The important point is that there is no general reason for expecting genetic influences to be any more irreversible than environmental ones.

I had forgotten the great computer myth, as well as the great gene myth, or I would have been more careful when I myself wrote of genes swarming ‘inside gigantic lumbering robots …’, and of ourselves as ‘survival machines—robot vehicles blindly programmed to preserve the selfish molecules known as genes’ (Dawkins 1976a). These passages have been triumphantly quoted, and requoted apparently from secondary and even tertiary sources, as examples of rabid genetic determinism

From 13 years’ experience of teaching it, I know that a main problem with the ‘selfish-gene survival machine’ way of looking at natural selection is a particular risk of misunderstanding

‘Genes for conformity, xenophobia, and aggressiveness are simply postulated for humans because they are needed for the theory, not because any evidence for them exists’

Pit-digging is a complex behaviour pattern. It costs time and energy, and satisfies the most exacting criteria for recognition as an adaptation (Williams 1966; Curio 1973). It must, then, have evolved by natural selection.

The adaptationism controversy is quite different. It is concerned with whether, given that we are dealing with a phenotypic effect big enough to see and ask questions about, we should assume that it is the product of natural selection.

One of the most impressive demonstrations of the subtlety of Charles Darwin’s mind is given by his discussion of winglessness and the costs of having wings in the insects of oceanic islands. For present purposes, the relevant point is that winged insects may risk being blown out to sea, and Darwin (1859, p. 177) suggested that this is why many island insects have reduced wings. But he also noted that some island insects are far from wingless; they have extra large wings.

However strongly adaptationist our beliefs may be, we can only expect animals to be average statistical optimizers, never perfect anticipators of every detail.

One of my purposes in this book is to question the ‘central theorem’ that it is useful to expect individual organisms to behave in such a way as to maximize their own inclusive fitness, or in other words to maximize the survival of copies of the genes inside them.

The argument is as follows. Biologists define behaviour as altruistic if it favours other individuals at the expense of the altruist himself.

I believe animals exert strong power over other animals, and that frequently an animal’s actions are most usefully interpreted as working in the interests of another individual’s inclusive fitness, rather than its own.

Schleidt (1973) discusses other examples of such ‘tonic’ effects of signals on the physiology of the receiver.

I think something along those lines is quite probably the explanation of the extraordinarily high rate of copulation observed in large cats (Eaton 1978). Schaller (1972) followed a sample male lion for 55 hours, during which he copulated 157 times, with an average inter-copulation interval of 21 minutes.

The optimon (or selecton) is the ‘something’ to which we refer when we speak of an adaptation as being ‘for the good of’ something.

I define a replicator as anything in the universe of which copies are made. Examples are a DNA molecule, and a sheet of paper that is xeroxed.

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.

A passive replicator is a replicator whose nature has no influence over its probability of being copied. A xeroxed sheet of paper at first sight seems to be an example, but some might argue that its nature does influence whether it is copied, and therefore that it is active: humans are more likely to xerox some sheets of paper than others, because of what is written on them, and these copies are, in their turn, relatively likely to be copied again.

I have previously summed up the qualities of a successful replicator ‘in a slogan reminiscent of the French Revolution: Longevity, Fecundity, Fidelity’ (Dawkins 1978a). Hull (1980b) explains the point clearly.

A successful replicator is one that succeeds in lasting, in the form of copies, for a very long time measured in generations, and succeeds in propagating many copies of itself.

Natural selection is the process by which replicators change in frequency in the population relative to their alleles.

If chromosomes were like bead necklaces, the argument runs, with crossing-over always breaking the necklace between beads and not within them, you might hope to define discrete replicators in the population, containing an integral number of cistrons. But since crossover can occur anywhere (Watson 1976), not just between beads, all hope of defining discrete units disappears.

adaptations are for the good of the individual organism. I am suggesting here that, since we must speak of adaptations as being for the good of something, the correct something is the active, germ-line replicator.

An active replicator is a chunk of genome that, when compared to its alleles, exerts phenotypic power over its world, such that its frequency increases or decreases relative to that of its alleles.

‘A nest is not a true replicator because a [non-genetic] “mutation” which occurs in the construction of a nest, for example the accidental incorporation of a pine needle instead of the usual grass, is not perpetuated in future “generations of nests”. Similarly, protein molecules are not replicators, nor is messenger RNA’

It is important to remember that mere immortality is not a sufficient qualification. A lineage, such as a sequence of parents and offspring from the long-unchanged brachiopod genus Lingula, is unending in the same sense, and to the same extent, as a lineage of genes.

If individuals live in a social climate in which imitation is common, this corresponds to a cellular climate rich in enzymes for copying DNA.

It is true that the relative survival success of a meme will depend critically on the social and biological climate in which it finds itself, and this climate will certainly be influenced by the genetic make-up of the population. But it will also depend on the memes that are already numerous in the meme-pool.

individual organisms are not 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.

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.

Living matter introduces a whole new set of rungs to the ladder of complexity: macromolecules folding themselves into their tertiary forms, intracellular membranes and organelles, cells, tissues, organs, organisms, populations, communities and ecosystems. A similar hierarchy of units embedded in larger units epitomizes the complex artificial products of living things—semiconductor crystals, transistors, integrated circuits, computers and embedded units that can only be understood in terms of ‘software’.

Functionally speaking, too, genes are gregarious. They have phenotypic effects on bodies, but they do not do so in isolation.

But the majority of models ordinarily called ‘group selection’, including all those reviewed by Wilson (1975), and most of those reviewed by Wade (1978), are implicitly treating groups as vehicles. The end result of the selection discussed is a change in gene frequencies, for example an increase of ‘altruistic genes’ at the expense of ‘selfish genes’. It is still genes that are regarded as the replicators which actually survive (or fail to survive) as a consequence of the (vehicle) selection process.

Selection simply cannot see genes and pick among them directly. It must use bodies as an intermediary. A gene is a bit of DNA hidden within a cell. Selection views bodies. It favors some bodies because they are stronger, better insulated, earlier in their sexual maturation, fiercer in combat, or more beautiful to behold … If, in favoring a stronger body, selection acted directly upon a gene for strength,

In a particular model of animal fighting, for example, Maynard Smith (1972, p. 19) postulated five alternative ‘strategies’ (programs): 1 Fight conventionally; retreat if opponent proves to be stronger or if opponent escalates. 2 Fight at escalated level. Retreat only if injured. 3 Start conventionally. Escalate only if opponent escalates. 4 Start conventionally. Escalate only if opponent continues to fight conventionally. 5 Fight at escalated level. Retreat before getting hurt if opponent does likewise.

In other words we must assume that the allele that survives best at any given locus tends to be the one that is best for the genome as a whole.

If all replicators ‘know’ that their only hope of getting into the next generation is via the orthodox bottleneck of individual reproduction, all will have the same ‘interests at heart’; survival of the shared body to reproductive age, successful courtship and reproduction of the shared body, and a successful outcome to the parental enterprise of the shared body.

A phenotypic effect of a gene is the joint product of itself and its environment, an environment which includes the rest of the genome.

This suggests that there is an enormously variable richness of genetic labelling in molecules of sweat.

Our definition of an outlaw makes reference to its provoking of modifiers at other loci which tend to suppress its phenotypic effects.

A ‘kin-selection gene’ is, in a sense, working for itself alone, but it benefits the other genes in its genome as well.