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Lack of potential mates has lead to "sloppy" gene control and risk of disease for humans
January 24, 2005
Our evolutionary ancestors' lack of choice in the mating game has left modern humans exposed to disease, according to new research published in the journal PLOS Biology tomorrow (Tuesday 25 January 2005). Key regions of our DNA, that control when genes are switched on and off, have been altered by around 140,000 naturally-occurring mutations over the last six million years, the researchers found.
This has left modern humans with 'sloppy' gene control mechanisms which can make us susceptible to diseases, or directly cause genetic diseases.
The researchers suggest that most of the 'mildly harmful' mutations occurred at a time when there was only a small population (10,000) of early Hominids, the two legged primates that were to later evolve into both humans and chimpanzees.
Had there been more early Hominids, and hence a greater choice of mates, most of these mutations would have been overridden by natural selection from a larger pool of available DNA.
This contrasts dramatically with rats and mice which, because of their larger ancestral population, have been able to maintain the integrity of their regulatory sections of DNA.
The researchers, from the Universities of Bath, Edinburgh and Sussex, made the finding after comparing control regions in human, rat, mouse and chimpanzee DNA.
After 'unwinding' evolution using statistical techniques, they found that the way our genes are switched on and off is much less carefully controlled in humans and chimpanzees compared to other animals.
"We are used to viewing us as the pinnacle of evolution but seeing that rodents control their genes much more precisely is somewhat sobering," said Dr Martin Lercher from the University of Bath.
"As a species we have become used to the benefits of ever-increasing health care and nutrition, but if what we found is still ongoing, then these improvements might at some point be offset by the deterioration of our gene control regions."
Bath, University of
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