Monday, September 10, 2007

Starch and human evolution

Nature Genetics has a paper out on the differences in copy number of a gene (AMY1) that is involved in starch digestion between humans and other primates. The authors extend the implications of their findings a bit too far however (or at least they do in the BBC writeup) in saying that starch was more responsible than meat in allowing for a large brain.
The part on between-population differences in humans is pretty cool.
Check out some previous posts with a similar theme: USOs in hominin diet (USOs- underground storage organs, such as potatoes etc...) and the role of cooking in human evolution.

Diet and the evolution of human amylase gene copy number variation

George H Perry, Nathaniel J Dominy, Katrina G Claw, Arthur S Lee, Heike Fiegler, Richard Redon, John Werner, Fernando A Villanea, Joanna L Mountain, Rajeev Misra, Nigel P Carter, Charles Lee & Anne C Stone

Nature Genetics Published online: 9 September 2007

Abstract: Starch consumption is a prominent characteristic of agricultural societies and hunter-gatherers in arid environments. In contrast, rainforest and circum-arctic hunter-gatherers and some pastoralists consume much less starch1, 2, 3. This behavioral variation raises the possibility that different selective pressures have acted on amylase, the enzyme responsible for starch hydrolysis4. We found that copy number of the salivary amylase gene (AMY1) is correlated positively with salivary amylase protein level and that individuals from populations with high-starch diets have, on average, more AMY1 copies than those with traditionally low-starch diets. Comparisons with other loci in a subset of these populations suggest that the extent of AMY1 copy number differentiation is highly unusual. This example of positive selection on a copy number–variable gene is, to our knowledge, one of the first discovered in the human genome. Higher AMY1 copy numbers and protein levels probably improve the digestion of starchy foods and may buffer against the fitness-reducing effects of intestinal disease.

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