Sex is something that most people think about on a minutely basis, but most don’t *really* think about it. From a macroscopic evolutionary view, sex doesn’t really make sense. The amount of effort that males put in to attract females, even outside the human species, is extreme. Sex is expensive in terms of time, effort, and stress. It would be much easier and less expensive from a reproduction standpoint to undergo binary fission, or drop pieces of oneself every time one wanted to reproduce.
Of course we don’t do that, and there are a few explanations as to why this is. (Because it’s “fun” doesn’t apply: that’s an evolutionary byproduct of needing to reproduce.) One hypothesis put forth almost 20 years ago suggests that sex evolved as a way to purge harmful mutations from the population. By shuffling genes “randomly” (mixing chromosomes is anything but random — any sociologist will tell you that), the harmful mutations would be concentrated into a few select individuals who would be weaker and less likely to reproduce, and therefore these mutations would be weeded out through natural selection.
We know now that this is way oversimplified. Most mutations occur in the non-coding (“junk”) DNA of an organism, and most genetic diseases are the product of many mutations, not just one. Then there is the fact that genetic disorders can be carried and passed on to offspring without every having been expressed. (For instance, when a disease “skips” a generation.) It turns out that observing this “negative epistasis” in nature has been rather difficult. Figuring out how it evolved has been even more challenging.
Now a new computer model provides a possible answer to this last question.
The researchers created digital organisms that reproduced through sex in the same manner as real organisms. And like a regular organism, the virtual one developed a natural buffer to resist change by mutations. This ability, called “genetic robustness,” is thought to be one of the main benefits of sex.
By shuffling genes, sex allows a population to spread its mutations across many individuals within a group. The mutations become diluted and can be effectively dealt with by an individual’s genetic repair system.
But the researchers found that the protection only works when the digital organisms were facing a few mutations at a time. When assaulted by many at once, their repair systems became overwhelmed and the organisms died. Azevedo think this happens in real life, too.
In essence there is a buffer: one or two mutations is okay, but once this buffer is overrun, negative epistasis takes over. The genetic robustness of sex and a limited ability to deal with mutations naturally leads to negative epistasis which protects a species at the cost of a few individuals within a population. How this actually truly gets rid of a disease, I’m not sure. If it were really an effective system one would think things like Huntington’s disease and Fragile X syndrome would have been weeded out long ago. I would be interested to see how negative epistasis effects carriers of disease instead of just those who express it.
[tags]negative epistasis, sex, sexual reproduction[/tags]