In order to promote themselves, certain genes resort to underhand tactics. Welcome to the realities of evolution
if there has been one major transformation over the past two decades in the way we look at evolution, it is the increasing trend to adopt a gene-centred view, instead of an individual-centred view or the old-fashioned -- and nearly defunct -- species-centred view. In other words, we see evolutionary change as something that happens never for 'the good of the species', sometimes for 'the good of the individual', and always for 'the good of the gene'.
To be sure, this viewpoint is not accepted universally. There are vigorous debates between supporters of the latter two points of view. Whatever the ultimate resolution of the debate, the fact remains that we have an impressive body of evidence that draws attention to the usefulness of looking at genes as the central characters in the play of life. The most striking single piece of evidence has to do with a gene known as segregation distorter ( Sd ).
The story begins 40 years ago. Y Hiraizumi and J F Crow attempted to mate male fruitflies ( Drosophila melanogaster ) caught in the wild with females, either from the wild or from strains developed in the laboratory . To their surprise, Hiraizumi and Crow discovered that some of these males produced exactly half the number of progeny that they should have. Closer investigation showed that the reason for this deficit was totally unexpected. The males that were affected passed on only a single copy of one of their chromosomes to their offspring. The other copy, it turned out, was being destroyed. Evidently, the normal law of 'genetic segregation', known since the time of the 19th century Moravian botanist Gregor Mendel, was being subverted or distorted. The law says that each of the two sister chromosomes in the parent has a 50 per cent chance of being passed on to any offspring. The agent responsible for this subversion was a gene, and was christened segregation distorter.
Simply put, one would call Sd a cheater gene because it cheats the system and gains an evolutionary advantage over its sister chromosome by pushing the sister out of the way, so to speak. Visually, one could see that the 'pushing out' was accomplished by preventing those spermatozoa that contained another gene called Responder gene ( Rsp ) from maturing fully. Such sperm never acquired the capability of successfully fertilising eggs. Clever genetic tricks could create chromosomes that contained both Sd and Rsp ; as one might have expected, such chromosomes committed suicide.
Soon the plot thickened. Not only was Sd a gene but its ability to get rid of the sister chromosome depended on the presence of the Rsp gene, this time located on the sister. So if one chromosome contains Sd and another contains Rsp , the Sd chromosome ensures that the Rsp chromosome is not passed on to the next generation. Two important questions follow. Firstly, why are Rsp -containing chromosomes present at all? The point is that evolution ought to have weeded them out if their possession is disadvantageous, as it certainly seems to be. Secondly, how exactly does this system of genetic skulduggery work?
The answer to the first question came some years ago. It is true that if any chromosome contains Sd , then a chromosome that has Rsp is worse off than one without. But Sd is a relatively rare gene -- in nature there are many flies that contain Rsp but no Sd . In these flies, for reasons that are not fully understood, the possession of Rsp seems to improve the fitness of the bearer. In experiments with a mixture of the two types of flies, the ones that possessed Rsp always increased in number over the ones that have no Rsp . The second question had not been answered in a satisfactory manner. Now, there is an explanation for it.
C Merrill and colleagues at the University of Wisconsin, usa , have at last succeeded in determining the dna sequence of the Sd gene. It turns out that the gene encodes a truncated version of a protein known as RanGAP. In short, the Sd product is a defective form of RanGAP. The usual complete form of the protein is expressed in the testes of the fly, where it helps sperm cells to mature. Under normal conditions, the transport of molecules into and out of the nucleus is helped by an enzyme known as Ran and the activity of Ran is stimulated by a second protein: RanGAP ( Science , Vol 283, No 2408).
What appears to be happening is that a defective version of RanGAP, resulting from a sperm nucleus carrying the Sd gene, causes improper transport of material in those sperm nuclei that carry the Rsp gene. Exactly how this happens is still unknown. But because a defective Sd is of no consequence if no other chromosome contains Rsp , whatever takes place must be an active process (and not just something that should happen but, on account of a defect in Sd, does not).
So, for the first time, we know what cheating in the genetic sense might entail. And while the exact interaction between Sd and Rsp still needs to be worked out, the present finding is a major step in our understanding of how genes are the leading actors in the process of evolution.
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