At some point in our past, our ancestors switched from the common reptilian habit of determining sex by the temperature of the egg to determining it genetically. The probable reason for the switch was so that each sex could start training for its special roleat conception. In our case, the sex-determining gene made us male and the lack of it left us female, whereas in birds it happened theother way round. The gene soon attracted to its side other genes that benefited males: genes for big muscles, say, or aggressive tendencies.But because these were not wanted in females — wasting energy they would prefer to spend on offspring – these secondary genes found themselves at an advantage in one sex and at a disadvantage in theother. They are known in the trade as sexually antagonistic genes.The dilemma was solved when another mutant gene suppressed the normal process of swapping of genetic material between thetwo paired chromosomes. Now the sexually antagonistic genes could diverge and go their different ways.
The version on the Y chromosome could use calcium to make antlers; the version on the Xchromosome could use calcium to make milk. Thus, a pair of middlesized chromosomes, once home to all sorts of ’normal‘ genes, was hijacked by the process of sex determination and became the sexchromosomes, each attracting different sets of genes. On the Y chromosome, genes accumulate that benefit males but are often bad for females; on the X accumulate genes that are good for females and deleterious in males.
For instance, there is a newly discovered gene called DAX, found on the X chromosome. A few rare people are born with one X and one Y chromosome, but with two copies of the DAX gene on the X chromosome. The result is, that although such people are genetically male, they develop into normal females. The reason, it transpires, is that DAX and SKY — the gene on theY chromosome that makes men into men — are antagonistic to each other. One SRY defeats one DAX, but two DAXes defeat one SRY.
This outbreak of antagonism between genes is a dangerous situation.Lurching into metaphor, one might begin to discern that the two chromosomes no longer have each other’s interests at heart, let alone those of the species as a whole. Or, to put it more correctly,something can be good for the spread of a gene on the X chromosomethat actually damages the Y chromosome or vice versa.Suppose, for instance, that a gene appeared on the X chromosome that specified the recipe for a lethal poison that killed only sperm carrying Y chromosomes. A man with such a gene would have no fewer children than another man. But he would have all daughters and no sons. All of those daughters would carry the new gene,whereas if he had had sons as well, none of them would have carried it. Therefore, the gene is twice as common in the next generationas it would otherwise be. It would spread very rapidly. Such a gene would only cease to spread when it had exterminated so many males that the very survival of the species was in jeopardy and males were at a high premium.
Far-fetched? Not at all. In the butterfly Acrea encedon, that is exactly what has happened. The sex ratio is ninety-seven per cent femaleas a result. This is just one of many cases known of this form of evolutionary conflict, known as sex-chromosome drive. Most known instances are confined to insects, but only because scientists have looked more closely at insects. The strange language of conflict usedin the remarks I quoted above now begins to make more sense. A piece of simple statistics: because females have two X chromosomes while males have an X and a Y, three-quarters of all sex chromosomes are Xs; one-quarter are Ys. Or, to put it another way, an X chromosome spends two-thirds of its time in females, and onlyone-third in males.Therefore, the X chromosome is three times aslikely to evolve the ability to take pot shots at the Y as the Y is to evolve the ability to take pot shots at the X. Any gene on the Ychromosome is vulnerable to attack by a newly evolved driving X gene.
The result has been that the Y chromosome has shed as many genes as possible and shut down the rest, to ‚run away and hide‘ (in the technical jargon used by William Amos of Cambridge University).So effectively has the human Y chromosome shut down most ofits genes that the great bulk of its length consists of non-codingDNA , serving no purpose at all – but giving few targets for the Xchromosome genes to aim at.
There is a small region that seems to have slipped across from the X chromosome fairly recently, theso-called pseudo-autosomal region, and then there is one immensely important gene, the SRY gene mentioned above. This gene begins the whole cascade of events that leads to the masculinisation of the embryo. Rarely can a single gene have acquired such power.Although it only throws a switch, much else follows from that. The genitals grow to look like a penis and testes, the shape and constitutionof the body are altered from female (the default in our species,though not in birds and butterflies), and various hormones go towork on the brain. There was a spoof map of the Y chromosomepublished in the journal Science a few years ago, which purported to have located genes for such stereotypically male traits as flipping between television channels, the ability to remember and tell jokes, an interest in the sports pages of newspapers, an addiction to death and destruction movies and an inability to express affection over the phone – among others.
The joke is funny, though, only becausewe recognise these habits as male, and therefore far from mocking the idea that such habits are genetically determined, the jokere inforces the idea. The only thing wrong with the diagram is that these male behaviours come not from specific genes for each of them, but from the general masculinisation of the brain by hormonessuch as testosterone which results in a tendency to behave this wayin the modern environment. Thus, in a sense, many masculine habits are all the products of the SRY gene itself, which sets in train theseries of events that lead to the masculinisation of the brain as wellas the body.
The SRY gene is peculiar. Its sequence is remarkably consistentbetween different men: there are virtually no point mutations (i.e.,one-letter spelling differences) in the human race. SRY is, in that sense, a variation-free gene that has changed almost not at all since the last common ancestor of all people 200,000 years ago or so. Yet our SRY is very different from that of a chimpanzee, and different again from that of a gorilla: there is, between species, ten times asmuch variation in this gene as is typical for other genes. Compared with other active (i.e., expressed) genes, SRY is one of the fastest evolving.
How do we explain this paradox? According to William Amosand John Harwood, the answer lies in the process of fleeing and hiding that they call selective sweeps. From time to time, a driving gene appears on the X chromosome that attacks the Y chromosome by recognising the protein made by SRY. At once there is a selective advantage for any rare SRY mutant that is sufficiently different tobe unrecognised. This mutant begins to spread at the expense of other males. The driving X chromosome distorts the sex ratio infavour of females but the spread of the new mutant SRY restoresthe balance. The end result is a brand new SRY gene sequence shared by all members of the species, with little variation.
The effect of this sudden burst of evolution (which might happen so quickly as to leave few traces in the evolutionary record) would be to produce SRYs that were very different between species, but very similar within species. If Amos and Harwood are right, at least one suchsweep must have occurred since the splitting of chimp ancestors and human ancestors, five to ten million years ago, but before theancestor common to all modern human beings, 200,000 years ago.
You may be feeling a little disappointed. The violence and conflict that I promised at the beginning of the chapter turn out to be little more than a detailed piece of molecular evolution. Fear not. I amnot finished yet, and I plan to link these molecules to real, human conflict soon enough.The leading scholar of sexual antagonism is William Rice of theUniversity of California at Santa Cruz and he has completed a remarkable series of experiments to make the point explicit. Let us go back to our putative ancestral creature that has just acquired a distinct Y chromosome and is in the process of shutting down many of the genes on it to escape driving X genes. This nascent Ychromosome, in Rice’s phrase, is now a hotspot for male-benefitgenes. Because a Y chromosome will never find itself in a female,it is free to acquire genes that are very bad for females so long asthey are at least slightly good for males (if you still thought evolution was about the good of the species, stop thinking so right now).
Infruit flies, and for that matter in human beings, male ejaculate consists of sperm cells suspended in a rich soup called the seminal fluid.Seminal fluid contains proteins, products of genes. Their purpose is entirely unknown, but Rice has a shrewd idea. During fruit-flysex, those proteins enter the bloodstream of the female and migrateto, among other places, her brain. There they have the effect of reducing the female’s sexual appetite and increasing her ovulation rate. Thirty years ago, we would have explained that increase interms of the good of the species. It is time for the female to stopseeking sexual partners and instead seek a nesting site. The male’sseminal fluid redirects her behaviour to that end. You can hear theNational Geographic commentary. Nowadays, this information takeson a more sinister aura. The male is trying to manipulate the femaleinto mating with no other males and into laying more eggs for hissperm and he is doing so at the behest of sexually antagonisticgenes, probably on the Y chromosome (or switched on by geneson the Y chromosome). The female is under selective pressure tobe more and more resistant to such manipulation. The outcome is a stalemate.
Rice did an ingenious experiment to test his idea. For twenty-nine generations, he prevented female flies from evolving resistance: he kept a separate strain of females in which no evolutionary change occurred. Meanwhile, he allowed males to generate more and moreeffective seminal fluid proteins by testing them against more and more resistant females. After twenty-nine generations he brought the two lines together again. The result was a walkover. Male sperm was now so effective at manipulating female behaviour that it was effectively toxic: it could kill the females.
Rice now believes that sexual antagonism is at work in all sorts of environments. It leaves its signature as rapidly evolving genes. In the shellfish the abalone, for instance, the lysin protein that the sperm uses to bore a hole through the glycoprotein matrix of the egg is encoded by a gene that changes very rapidly (the same isprobably true in us), probably because there is an arms race betweenthe lysin and the matrix. Rapid penetration is good for sperm but bad for the egg, because it allows parasites or second sperm through.Coming slightly closer to home, the placenta is controlled by rapidly evolving genes (and paternal ones, at that). Modern evolutionary theorists, led by David Haig, now think of the placenta as more likea parasitic takeover of the mother’s body by paternal genes in the foetus. The placenta tries, against maternal resistance, to control herblood-sugar levels and blood pressure to the benefit of the foetus. More on this in the chapter on chromosome 15.
But what about courtship behaviour? The traditional view of the peacock’s elaborate tail is that it is a device designed to seducefemales and that it is in effect designed by ancestral females‘ preferences.Rice’s colleague, Brett Holland, has a different explanation.He thinks peacocks did indeed evolve long tails to seduce females,but that they did so because females grew more and more resistantto being so seduced. Males in effect use courtship displays as asubstitute for physical coercion and females use discrimination toretain control over their own frequency and timing of mating. Thisexplains a startling result from two species of wolf spiders. Onespecies has tufts of bristles on its forelegs that it uses in courtship.Shown a video of a male spider displaying, the female will indicate by her behaviour whether the display turns her on. If the videos are altered so that the males‘ tufts disappear, the female is still just as likely to find the display arousing. But in another species, where there are no tufts, the artificial addition of tufts to males on the video more than doubled the acceptance rate of females. In otherwords, females gradually evolve so that they are turned off, not on,by the displays of males of their own species. Sexual selection is thus an expression of sexual antagonism between genes for seduction and genes for resistance.
Rice and Holland come to the disturbing conclusion that the more social and communicative a species is, the more likely it is to suffer from sexually antagonistic genes, because communication between the sexes provides the medium in which sexually antagonisticgenes thrive. The most social and communicative species on the planet is humankind.
Suddenly it begins to make sense why relations between the human sexes are such a minefield, and why men have such vastly different interpretations of what constitutes sexual harassment from women. Sexual relations are driven not by what is good, in evolutionary terms, for men or for women, but for their chromosomes. The ability to seduce a woman was good for Y chromosomes in the past; the ability to resist seduction by a man was good for X chromosomes in the past.
This kind of conflict between complexes of genes (the Y chromosome being one such complex), does not just apply to sex. Suppose that there is a version of a gene that increases the telling of lies (not a very realistic proposition, but there might be a large set of genes that affect truthfulness indirectly). Such a gene might thrive by making its possessors into successful con-artists. But then suppose there is also a version of a different gene (or set of genes) that improves the detecting of lies, perhaps on a different chromosome.That gene would thrive to the extent that it enabled its possessors to avoid being taken in by con-artists. The two would evolve antagonistically,each gene encouraging the other, even though it wouldbe quite possible for the same person to possess both. There is between them what Rice and Holland call ‚interlocus contest or ICE.
Exactly such a competitive process probably did indeed drive the growth of human intelligence over the past three million years. The notion that our brains grew big to help us make tools or start fires on the savannah has long since lost favour.Instead, most evolutionists believe in the Machiavellian theory —that bigger brains were needed in an arms race between manipulationand resistance to manipulation. ‚The phenomena we refer to as intelligence may be a byproduct of intergenomic conflict between genes mediating offense and defense in the context of language‘,write Rice and Holland.
Eure Meinung dazu würde mich interessieren.
Mir kommen in dem Text noch ein paar andere Aspekte zu kurz, etwa direkte sexuelle Selektion und ihre Auswirkungen auf die Partnerwahl und den Umstand, dass es nach der Sexy Son Theorie noch eine Ebene gibt, bei der die Fähigkeit das andere Geschlecht auszutricken, selbst sexy sein kann, also negative Umstände unter gewissen Umständen positive werden können, aber in dem Text ist dennoch sehr viel drin.