The Selfish Gene (37 page)

We can take this argument to its logical conclusion and apply it to normal, 'own' genes. Our own genes cooperate with one another, not because they are our own but because they share the same outlet- sperm or egg-into the future. If any genes of an organism, such as a human, could discover a way of spreading themselves that did not depend on the conventional sperm or egg route, they would take it and be less cooperative. This is because they would stand to gain by a different set of future outcomes from the other genes in the body. We've already seen examples of genes that bias meiosis in their own favour. Perhaps there are also genes that have broken out of the sperm/egg 'proper channels' altogether and pioneered a sideways route.

There are fragments of DNA that are not incorporated in chromosomes but float freely and multiply in the fluid contents of cells, especially bacterial cells. They go under various names such as viroids or plasmids. A plasmid is even smaller than a virus, and it normally consists of only a few genes. Some plasmids are capable of splicing themselves seamlessly into a chromosome. So smooth is the splice that you can't see the join: the plasmid is indistinguishable from any other part of the chromosome. The same plasmids can also cut themselves out again. This ability of DNA to cut and splice, to jump in and out of chromosomes at the drop of a hat, is one of the more exciting facts that have come to light since the first edition of this book was published. From some points of view it does not really matter whether these fragments originated as invading parasites or breakaway rebels. Their likely behaviour will be the same. I shall talk about a breakaway fragment in order to emphasize my point.

Consider a rebel stretch of human DNA that is capable of snipping itself out of its chromosome, floating freely in the cell, perhaps multiplying itself up into many copies, and then splicing itself into another chromosome. What unorthodox alternative routes into the future could such a rebel replicator exploit? We are losing cells continually from our skin; much of the dust in our houses consists of our sloughed-off cells. We must be breathing in one another's cells all the time. If you draw your fingernail across the inside of your mouth it will come away with hundreds of living cells. The kisses and caresses of lovers must transfer multitudes of cells both ways. A stretch of rebel DNA could hitch a ride in any of these cells. If genes could discover a chink of an unorthodox route through to another body (alongside, or instead of, the orthodox sperm or egg route), we must expect natural selection to favour their opportunism and improve it. As for the precise methods that they use, there is no reason why these should be any different from the machinations-all too predictable to a selfish gene/extended phenotype theorist-of viruses.

When we have a cold or a cough, we normally think of the symptoms as annoying byproducts of the virus's activities. But in some cases it seems more probable that they are deliberately engineered by the virus to help it to travel from one host to another. Not content with simply being breathed into the atmosphere, the virus makes us sneeze or cough explosively. The rabies virus is transmitted in saliva when one animal bites another. In dogs, one of the symptoms of the disease is that normally peaceful and friendly animals become ferocious biters, foaming at the mouth. Ominously too, instead of staying within a mile or so of home like normal dogs, they turn into restless wanderers, propagating the virus far afield. It has even been suggested that the well-known hydrophobic symptom encourages the dog to shake the wet foam from its mouth-and with it the virus. I do not know of any direct evidence that sexually transmitted diseases increase the libido of sufferers, but I conjecture that it would be worth looking into. Certainly at least one alleged aphrodisiac, Spanish Fly, is said to work by inducing an itch .. . and making people itch is just the kind of thing viruses are good at.

The point of comparing rebel human DNA with invading parasitic viruses is that there really isn't any important difference between them. Viruses may well, indeed, have originated as collections of breakaway genes. If we want to erect any distinction, it should be between genes that pass from body to body via the orthodox route of sperms or eggs, and genes that pass from body to body via unorthodox, 'sideways' routes. Both classes may include genes that originated as 'own' chromosomal genes. And both classes may include genes that originated as external, invading parasites. Or perhaps all 'own' chromosomal genes should be regarded as mutually parasitic on one another. The important difference between my two classes of genes lies in the divergent circumstances from which they stand to benefit in the future. A cold virus gene and a breakaway human chromosomal gene agree with one another in 'wanting' their host to sneeze. An orthodox chromosomal gene and a venereally transmitted virus agree with one another in wanting their host to copulate. It is an intriguing thought that both would want the host to be sexually attractive. More, an orthodox chromosomal gene and a virus that is transmitted inside the host's egg would agree in wanting the host to succeed not just in its courtship but in every detailed aspect of its life, down to being a loyal, doting parent and even grandparent.

The caddis lives inside its house, and the parasites that I have so far discussed have lived inside their hosts. The genes, then, are physically close to their extended phenotypic effects, as close as genes ordinarily are to their conventional phenotypes. But genes can act at a distance; extended phenotypes can extend a long way. One of the longest that I can think of spans a lake. Like a spider web or a caddis house, a beaver dam is among the true wonders of the world.

It is not entirely clear what its Darwinian purpose is, but it certainly must have one, for the beavers expend so much time and energy to build it. The lake that it creates probably serves to protect the beaver's lodge from predators. It also provides a convenient waterway for travelling and for transporting logs. Beavers use flotation for the same reason as Canadian lumber companies use rivers and eighteenth-century coal merchants used canals. Whatever its benefits, a beaver lake is a conspicuous and characteristic feature of the landscape. It is a phenotype, no less than the beaver's teeth and tail, and it has evolved under the influence of Darwinian selection. Darwinian selection has to have genetic variation to work on. Here the choice must have been between good lakes and less good lakes. Selection favoured beaver genes that made good lakes for transporting trees, just as it favoured genes that made good teeth for felling them. Beaver lakes are extended phenotypic effects of beaver genes, and they can extend over several hundreds of yards. A long reach indeed!

Parasites, too, don't have to live inside their hosts; their genes can express themselves in hosts at a distance. Cuckoo nestlings don't live inside robins or reed-warblers; they don't suck their blood or devour their tissues, yet we have no hesitation in labelling them as parasites. Cuckoo adaptations to manipulate the behaviour of foster-parents can be looked upon as extended phenotypic action at a distance by cuckoo genes.

It is easy to empathize with foster parents duped into incubating the cuckoo's eggs. Human egg collectors, too, have been fooled by the uncanny resemblance of cuckoo eggs to, say, meadow-pipit eggs or reed-warbler eggs (different races of female cuckoos specialize in different host species). What is harder to understand is the behaviour of foster-parents later in the season, towards young cuckoos that are almost fledged. The cuckoo is usually much larger, in some cases grotesquely larger, than its 'parent'. I am looking at a photograph of an adult dunnock, so small in comparison to its monstrous foster-child that it has to perch on its back in order to feed it. Here we feel less sympathy for the host. We marvel at its stupidity, its gullibility. Surely any fool should be able to see that there is something wrong with a child like that.

I think that cuckoo nestlings must be doing rather more than just 'fooling' their hosts, more than just pretending to be something that they aren't. They seem to act on the host's nervous system in rather the same way as an addictive drug. This is not so hard to sympathize with, even for those with no experience of addictive drugs. A man can be aroused, even to erection, by a printed photograph of a woman's body. He is not 'fooled' into thinking that the pattern of printing ink really is a woman. He knows that he is only looking at ink on paper, yet his nervous system responds to it in the same kind of way as it might respond to a real woman. We may find the attractions of a particular member of the opposite sex irresistible, even though the better judgment of our better self tells us that a liaison with that person is not in anyone's long-term interests. The same can be true of the irresistible attractions of unhealthy food. The dunnock probably has no conscious awareness of its long-term best interests, so it is even easier to understand that its nervous system might find certain kinds of stimulation irresistible.

So enticing is the red gape of a cuckoo nestling that it is not uncommon for ornithologists to see a bird dropping food into the mouth of a baby cuckoo sitting in some other bird's nest! A bird may be flying home, carrying food for its own young. Suddenly, out of the corner of its eye, it sees the red super-gape of a young cuckoo, in the nest of a bird of some quite different species. It is diverted to the alien nest where it drops into the cuckoo's mouth the food that had been destined for its own young. The 'irresistibility theory' fits with the views of early German ornithologists who referred to foster-parents as behaving like 'addicts' and to the cuckoo nestling as their 'vice'. It is only fair to add that this kind of language finds less favour with some modern experimenters. But there's no doubt that if we do assume that the cuckoo's gape is a powerful drug-like super-stimulus, it becomes very much easier to explain what is going on. It becomes easier to sympathize with the behaviour of the diminutive parent standing on the back of its monstrous child. It is not being stupid. 'Fooled' is the wrong word to use. Its nervous system is being controlled, as irresistibly as if it were a helpless drug addict, or as if the cuckoo were a scientist plugging electrodes into its brain.

But even if we now feel more personal sympathy for the manipulated foster-parent, we can still ask why natural selection has allowed the cuckoos to get away with it. Why haven't host nervous systems evolved resistance to the red gape drug? Maybe selection hasn't yet had time to do its work. Perhaps cuckoos have only in recent centuries started parasitizing their present hosts, and will in a few centuries be forced to give them up and victimize other species.

There is some evidence to support this theory. But I can't help feeling that there must be more to it than that.

In the evolutionary 'arms race' between cuckoos and any host species, there is a sort of built-in unfairness, resulting from unequal costs of failure. Each individual cuckoo nestling is descended from a long line of ancestral cuckoo nestlings, every single one of whom must have succeeded in manipulating its foster-parent. Any cuckoo nestling that lost its hold, even momentarily, over its host would have died as a result. But each individual foster-parent is descended from a long line of ancestors many of whom never encountered a cuckoo in their lives. And those that did have a cuckoo in their nest could have succumbed to it and still lived to rear another brood next season. The point is that there is an asymmetry in the cost of failure. Genes for failure to resist enslavement by cuckoos can easily be passed down the generations of robins or dunnocks. Genes for failure to enslave foster-parents cannot be passed down the generations of cuckoos. This is what I meant by 'built-in unfairness', and by 'asymmetry in the cost of failure'. The point is summed up in one of Aesop's fables: 'The rabbit runs faster than the fox, because the rabbit is running for his life while the fox is only running for his dinner.' My colleague John Krebs and I have dubbed this the 'life/ dinner principle'.

Because of the life/dinner principle, animals might at times behave in ways that are not in their own best interests, manipulated by some other animal. Actually, in a sense they are acting in their own best interests: the whole point of the life/dinner principle is that they theoretically could resist manipulation but it would be too costly to do so. Perhaps to resist manipulation by a cuckoo you need bigger eyes or a bigger brain, which would have overhead costs. Rivals with a genetic tendency to resist manipulation would actually be less successful in passing on genes, because of the economic costs of resisting.

But we have once again slipped back into looking at life from the point of view of the individual organism rather than its genes. When we talked about flukes and snails we accustomed ourselves to the idea that a parasite's genes could have phenotypic effects on the host's body, in exactly the same way as any animal's genes have phenotypic effects on its 'own' body. We showed that the very idea of an 'own' body was a loaded assumption. In one sense, all the genes in a body are 'parasitic' genes, whether we like to call them the body's 'own' genes or not. Cuckoos came into the discussion as an example of parasites not living inside the bodies of their hosts. They manipulate their hosts in much the same way as internal parasites do, and the manipulation, as we have now seen, can be as powerful and irresistible as any internal drug or hormone. As in the case of internal parasites, we should now rephrase the whole matter in terms of genes and extended phenotypes.

In the evolutionary arms race between cuckoos and hosts, advances on each side took the form of genetic mutations arising and being favoured by natural selection. Whatever it is about the cuckoo's gape that acts like a drug on the host's nervous system, it must have originated as a genetic mutation. This mutation worked via its effect on, say, the colour and shape of the young cuckoo's gape. But even this was not its most immediate effect. Its most immediate effect was upon unseen chemical happenings inside cells.