Get the Mosquitoes!
- Genes in Conflict: The Biology of Selfish Genetic Elements by Austin Burt and Robert Trivers
Harvard, 602 pp, £21.95, January 2006, ISBN 0 674 01713 7
Some flour beetles carry a gene called Medea. Their offspring look normal as larvae but, around the time of hatching, half the females become listless, then paralysed; and then they die. No one knows how it works, but the female offspring that inherit a copy of the gene are protected from the poison it uses, while those that don’t are killed by it.
Medea has evolved thanks to sexual reproduction. Nearly all animals carry two copies of each chromosome (in plants and fungi the situation is more complicated, but the principles are largely the same). Some genes are present in a different version on each copy, which is why someone can carry the gene that causes cystic fibrosis or sickle-cell anaemia, but not suffer from the disease. These genes are recessive, which means their effects show themselves only if they are present on both copies of a chromosome. When eggs and sperm are created, however, the genome is first shuffled to form a new combination of genes from both parents, and then halved, so that only one copy of each chromosome from each parent makes it into the next generation. This is why, when two carriers of the cystic fibrosis gene reproduce, there is only a 25 per cent likelihood of their children suffering from the disease (and a 50 per cent chance of their being carriers).
Most genes put up with this reproductive lottery: the evolutionary cost of being absent from half of the next generation looks to have been outweighed by the benefits of sexual reproduction as a quick way to bring good genes together and weed bad ones out. But any gene that can rig the lottery, so that it gets into more than half its carrier’s offspring, will spread. These genes are not merely selfish in Richard Dawkins’s sense of being selected to out-compete different versions of themselves in the population: they are ruthless because, as in the case of Medea, they can spread even though their effects are strongly detrimental to the evolutionary interests of the organisms that carry them. Austin Burt and Robert Trivers call such genes ‘selfish genetic elements’.
That such elements should evolve is no more surprising than that viruses should exist. An organism results from the co-operation of a set of genes, and natural selection favours those organisms whose genes best equip them to reproduce. But, like co-operative systems everywhere, the genome is vulnerable to invasion by freeloaders. Sexual reproduction creates one sort of opportunity for these parasites to evolve, but there are others: bacteria, which do not reproduce sexually, nevertheless have genes that can kill daughter cells to which they have not been transmitted.
The existence of selfish genetic elements shows that natural selection goes on not only between organisms, but within them. The non-selfish genes, such as those that lose relatives in the beetles killed by Medea, will be selected to neutralise a selfish gene’s effects. Many organisms seem to carry selfish genetic elements whose effects are hidden by other genes; and, more generally, many features of the cellular machinery look as if they might be adaptations to counteract the forces of internal selection.
The way in which mitochondria are inherited, for example, looks as if it might have been an adaptation to deny opportunities for one part of an organism’s genome to turn on another. Mitochondria are cellular structures that power respiration, and are descended from a bacterium that fused with our ancestors about one billion years ago. They divide independently of the rest of the cell and have kept hold of a small chromosome separate from those in the nucleus. In nearly all species, mitochondria pass down only in the female line: our mitochondria are descended from those in our mother’s egg. In mammals, the mitochondria in sperm cells are marked with a protein tag that causes them to be destroyed after fertilisation.
Mixing mitochondria from two individuals in one egg cell would be like planting two strains of grass in one plot: each would be selected to out-compete the other. The strain that divided more quickly would be favoured, even if this harmed the host’s respiratory functions. Studies in yeast have shown that such mutations are common, and that they can spread to the detriment of the cells that carry them. The most plausible explanation for the uniparental inheritance of mitochondria is that the nuclear genomes of the two mates co-operate to reduce the chance that their offspring’s mitochondria will turn selfish.
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