The Selfish Gene Page 31
In fact, what Fischer observed was that the fishes operate a system of pretty strict alternation. This is just what we should expect if they are playing Tit for Tat. And it is plausible that they should, because it does appear that the game is a true Prisoner's Dilemma, albeit a somewhat complicated one. To play the cooperate card means to play the female role when it is your turn to do so. Attempting to play the male role when it is your turn to play the female is equivalent to playing the defect card. Defection is vulnerable to retaliation: the partner can refuse to play the female role next time it is 'her' (his?) turn to do so, or 'she' can simply terminate the whole relationship. Fischer did indeed observe that pairs with an uneven sharing of sex roles tended to break up.
A question that sociologists and psychologists sometimes ask is why blood donors (in countries, such as Britain, where they are not paid) give blood. I find it hard to believe that the answer lies in reciprocity or disguised selfishness in any simple sense. It is not as though regular blood donors receive preferential treatment when they come to need a transfusion. They are not even issued with little gold stars to wear. Maybe I am naive, but I find myself tempted to see it as a genuine case of pure, disinterested altruism. Be that as it may, blood-sharing in vampire bats seems to fit the Axelrod model well. We learn this from the work of G. S. Wilkinson.
Vampires, as is well known, feed on blood at night. It is not easy for them to get a meal, but if they do it is likely to be a big one. When dawn comes, some individuals will have been unlucky and return completely empty, while those individuals that have managed to find a victim are likely to have sucked a surplus of blood. On a subsequent night the luck may run the other way. So, it looks like a promising case for a bit of reciprocal altruism. Wilkinson found that those individuals who struck lucky on any one night did indeed sometimes donate blood, by regurgitation, to their less fortunate comrades. Out of 110 regurgitations that Wilkinson witnessed, 77 could easily be understood as cases of mothers feeding their children, and many other instances of blood-sharing involved other kinds of genetic relatives. There still remained, however, some examples of blood-sharing among unrelated bats, cases where the 'blood is thicker than water' explanation would not fit the facts. Significantly the individuals involved here tended to be frequent roostmates-they had every opportunity to interact with one another repeatedly, as is required for an Iterated Prisoner's Dilemma. But were the other requirements for a Prisoner's Dilemma met? The payoff matrix in Figure D is what we should expect if they were.
Figure D. Vampire bat blood-donor scheme: payoffs to me from various outcomes.
Do vampire economics really conform to this table? Wilkinson looked at the rate at which starved vampires lose weight. From this he calculated the time it would take a sated bat to starve to death, the time it would take an empty bat to starve to death, and all intermediates. This enabled him to cash out blood in the currency of hours of prolonged life. He found, not really surprisingly, that the exchange rate is different, depending upon how starved a bat is. A given amount of blood adds more hours to the life of a highly starved bat ' than to a less starved one. In other words, although the act of donating blood would increase the chances of the donor dying, this increase was small compared with the increase in the recipient's chances of surviving. Economically speaking, then, it seems plausible that vampire economics conform to the rules of a Prisoner's Dilemma. The blood that the donor gives up is less precious to her (social groups in vampires are female groups) than the same quantity of blood is to the recipient. On her unlucky nights she really would benefit enormously from a gift of blood. But on her lucky nights she would benefit slightly, if she could get away with it, from defecting- refusing to donate blood. 'Getting away with it', of course, means something only if the bats are adopting some kind of Tit for Tat strategy. So, are the other conditions for the evolution of Tit for Tat reciprocation met?
In particular, can these bats recognize one another as individuals? Wilkinson did an experiment with captive bats, proving that they can. The basic idea was to take one bat away for a night and starve it while the others were all fed. The unfortunate starved bat was then returned to the roost, and Wilkinson watched to see who, if anyone, gave it food. The experiment was repeated many times, with the bats taking turns to be the starved victim. The key point was that this population of captive bats was a mixture of two separate groups, taken from caves many miles apart. If vampires are capable of recognizing their friends, the experimentally starved bat should turn out to be fed only by those from its own original cave.
That is pretty much what happened. Thirteen cases of donation were observed. In twelve out of these thirteen, the donor bat was an 'old friend' of the starved victim, taken from the same cave; in only one out of the thirteen cases was the starved victim fed by a 'new friend', not taken from the same cave. Of course this could be a coincidence but we can calculate the odds against this. They come to less than one in 500. It is pretty safe to conclude that the bats really
were biased in favour of feeding old friends rather than strangers from a different cave.
Vampires are great mythmakers. To devotees of Victorian Gothic they are dark forces that terrorize by night, sapping vital fluids, sacrificing an innocent life merely to gratify a thirst. Combine this with that other Victorian myth, nature red in tooth and claw, and aren't vampires the very incarnation of deepest fears about the world of the selfish gene? As for me, I am sceptical of all myths. If we want to know where the truth lies in particular cases, we have to look. What the Darwinian corpus gives us is not detailed expectations about particular organisms. It gives us something subtler and more valuable: understanding of principle. But if we must have myths, the real facts about vampires could tell a different moral tale. To the bats themselves, not only is blood thicker than water. They rise above the bonds of kinship, forming their own lasting ties of loyal blood-brotherhood. Vampires could form the vanguard of a comfortable new myth, a myth of sharing, mutualistic cooperation. They could herald the benignant idea that, even with selfish genes at the helm, nice guys can finish first.
The long reach of the gene
An uneasy tension disturbs the heart of the selfish gene theory. It is the tension between gene and individual body as fundamental agent of life. On the one hand we have the beguiling image of independent DNA replicators, skipping like chamois, free and untrammelled down the generations, temporarily brought together in throwaway survival machines, immortal coils shuffling off an endless succession of mortal ones as they forge towards their separate eternities. On the other hand we look at the individual bodies themselves and each one is obviously a coherent, integrated, immensely complicated machine, with a conspicuous unity of purpose. A body doesn't look like the product of a loose and temporary federation of warring genetic agents who hardly have time to get acquainted before embarking in sperm or egg for the next leg of the great genetic diaspora. It has one single-minded brain which coordinates a cooperative of limbs and sense organs to achieve one end. The body looks and behaves like a pretty impressive agent in its own right.
In some chapters of this book we have indeed thought of the individual organism as an agent, striving to maximize its success in passing on all its genes. We imagined individual animals making complicated economic 'as if' calculations about the genetic benefits of various courses of action. Yet in other chapters the fundamental rationale was presented from the point of view of genes. Without the gene's-eye view of life there is no particular reason why an organism should 'care' about its reproductive success and that of its relatives, rather than, for instance, its own longevity.
How shall we resolve this paradox of the two ways of looking at life? My own attempt to do so is spelled out in The Extended Phenotype, the book that, more than anything else I have achieved in my professional life, is my pride and joy. This chapter is a brief distillation of a few of the themes in that book, but really I'd almost rather you stopped reading now and switched to The Extended Phenotype!
On any sensible view of the matter Darwinian selection does not work on genes directly. DNA is cocooned in protein, swaddled in membranes, shielded from the world and invisible to natural selection. If selection tried to choose DNA molecules directly it would hardly find any criterion by which to do so. All genes look alike, just as all recording tapes look alike. The important differences between genes emerge only in their effects. This usually means effects on the processes of embryonic development and hence on bodily form and behaviour. Successful genes are genes that, in the environment influenced by all the other genes in a shared embryo, have beneficial effects on that embryo. Beneficial means that they make the embryo likely to develop into a successful adult, an adult likely to reproduce and pass those very same genes on to future generations. The technical word Phenotype is used for the bodily manifestation of a gene, the effect that a gene, in comparison with its alleles, has on the body, via development. The phenotypic effect of some particular gene might be, say, green eye colour. In practice most genes have more than one phenotypic effect, say green eye colour and curly hair. Natural selection favours some genes rather than others not because of the nature of the genes themselves, but because of their consequences-their phenotypic effects.
Darwinians have usually chosen to discuss genes whose phenotypic effects benefit, or penalize, the survival and reproduction of whole bodies. They have tended not to consider benefits to the gene itself. This is partly why the paradox at the heart of the theory doesn't normally make itself felt. For instance a gene may be successful through improving the running speed of a predator. The whole predator's body, including all its genes, is more successful because it runs faster. Its speed helps it survive to have children; and therefore more copies of all its genes, including the gene for fast running, are passed on. Here the paradox conveniently disappears because what is good for one gene is good for all.
But what if a gene exerted a phenotypic effect that was good for itself but bad for the rest of the genes in the body? This is not a flight of fancy. Cases of it are known, for instance the intriguing phenomenon called meiotic drive. Meiosis, you will remember, is the special kind of cell division that halves the number of chromosomes and gives rise to sperm cells or egg cells. Normal meiosis is a completely fair lottery. Of each pair of alleles, only one can be the lucky one that enters any given sperm or egg. But it is equally likely to be either one of the pair, and if you average over lots of sperms (or eggs) it turns out that half of them contain one allele, half the other. Meiosis is fair, like tossing a penny. But, though we proverbially think of tossing a penny as random, even that is a physical process influenced by a multitude of circumstances-the wind, precisely how hard the penny is flicked, and so on. Meiosis, too, is a physical process, and it can be influenced by genes. What if a mutant gene arose that just happened to have an effect, not upon something obvious like eye colour or curliness of hair, but upon meiosis itself? Suppose it happened to bias meiosis in such a way that it, the mutant gene itself, was more likely than its allelic partner to end up in the egg. There are such genes and they are called segregation distorters. They have a diabolical simplicity. When a segregation distorter arises by mutation, it will spread inexorably through the population at the expense of its allele. It is this that is known as meiotic drive. It will happen even if the effects on bodily welfare, and on the welfare of all the other genes in the body, are disastrous.
Throughout this book we have been alert to the possibility of individual organisms 'cheating' in subtle ways against their social companions. Here we are talking about single genes cheating against the other genes with which they share a body. The geneticist James Crow has called them 'genes that beat the system'. One of the best-known segregation distorters is the so-called t gene in mice. When a mouse has two t genes it either dies young or is sterile, t is therefore said to be lethal in the homozygous state. If a male mouse has only one t gene it will be a normal, healthy mouse except in one remarkable respect. If you examine such a male's sperms you will find that up to 95 per cent of them contain the t gene, only 5 per cent the normal allele. This is obviously a gross distortion of the 50 per cent ratio that we expect. Whenever, in a wild population, a t allele happens to arise by mutation, it immediately spreads like a brushfire. How could it not, when it has such a huge unfair advantage in the meiotic lottery? It spreads so fast that, pretty soon, large numbers of individuals in the population inherit the t gene in double dose (that is, from both their parents). These individuals die or are sterile, and before long the whole local population is likely to be driven extinct. There is some evidence that wild populations of mice have, in the past, gone extinct through epidemics of t genes.
Not all segregation distorters have such destructive side-effects as t. Nevertheless, most of them have at least some adverse consequences. (Almost all genetic side-effects are bad, and a new mutation will normally spread only if its bad effects are outweighed by its good effect. If both good and bad effects apply to the whole body, the net effect can still be good for the body. But if the bad effects are on the body, and the good effects are on the gene alone, from the body's point of view the net effect is all bad.) In spite of its deleterious side-effects, if a segregation distorter arises by mutation it will surely tend to spread through the population. Natural selection (which, after all, works at the genic level) favours the segregation distorter, even though its effects at the level of the individual organism are likely to be bad.
Although segregation distorters exist they aren't very common. We could go on to ask why they aren't common, which is another way of asking why the process of meiosis is normally fair, as scrupulously impartial as tossing a good penny. We'll find that the answer drops out once we have understood why organisms exist anyway.
The individual organism is something whose existence most biologists take for granted, probably because its parts do pull together in such a united and integrated way. Questions about life are conventionally questions about organisms. Biologists ask why organisms do this, why organisms do that. They frequently ask why organisms group themselves into societies. They don't ask-though they should-why living matter groups itself into organisms in the first place. Why isn't the sea still a primordial battleground of free and independent replicators? Why did the ancient replicators club together to make, and reside in, lumbering robots, and why are those robots-individual bodies, you and me-so large and so complicated?
It is hard for many biologists even to see that there is a question here at all. This is because it is second nature for them to pose their questions at the level of the individual organism. Some biologists go so far as to see DNA as a device used by organisms to reproduce themselves, just as an eye is a device used by organisms to see! Readers of this book will recognize that this attitude is an error of great profundity. It is the truth turned crashingly on its head. They will also recognize that the alternative attitude, the selfish gene view of life, has a deep problem of its own. That problem-almost the reverse one-is why individual organisms exist at all, especially in a form so large and coherently purposeful as to mislead biologists into turning the truth upside down. To solve our problem, we have to begin by purging our minds of old attitudes that covertly take the individual organism for granted; otherwise we shall be begging the question. The instrument with which we shall purge our minds is the idea that I call the extended phenotype. It is to this, and what it means, that I now turn.
The phenotypic effects of a gene are normally seen as all the effects that it has on the body in which it sits. This is the conventional definition. But we shall now see that the phenotypic effects of a gene need to be thought of as all the effects that it has on the world. It may be that a gene's effects, as a matter of fact, turn out to be confined to the succession of bodies in which the gene sits. But, if so, it will be just as a matter of fact. It will not be something that ought to be part of our very definition. In all this, remember that the phenotypic effects of a gene are the tools by which it leve
rs itself into the next generation. All that I am going to add is that the tools may reach outside the individual body wall. What might it mean in practice to speak of a gene as having an extended phenotypic effect on the world outside the body in which it sits? Examples that spring to mind are artefacts like beaver dams, bird nests and caddis houses.
Caddis flies are rather nondescript, drab brown insects, which most of us fail to notice as they fly rather clumsily over rivers. That is when they are adults. But before they emerge as adults they have a rather longer incarnation as larvae walking about the river bottom. And caddis larvae are anything but nondescript. They are among the most remarkable creatures on earth. Using cement of their own manufacture, they skilfully build tubular houses for themselves out of materials that they pick up from the bed of the stream. The house is a mobile home, carried about as the caddis walks, like the shell of a snail or hermit crab except that the animal builds it instead of growing it or finding it. Some species of caddis use sticks as building materials, others fragments of dead leaves, others small snail shells. But perhaps the most impressive caddis houses are the ones built in local stone. The caddis chooses its stones carefully, rejecting those that are too large or too small for the current gap in the wall, even rotating each stone until it achieves the snuggest fit.