In the classical view of evolution, species experience spontaneous genetic mutations that produce various novel traits—some helpful, some detrimental. Nature then selects for those most beneficial, passing them along to subsequent generations. It’s an elegant model. It’s also an extremely time-consuming process likely to fail organisms needing to cope with sudden, potentially life-threatening changes in their environments. Surely some other mechanism could enable more rapid adaptive response. In this week’s edition of the journal Science, a team of researchers from Harvard Medical School and Whitehead Institute report that, at least in the case of one variety of cavefish, that other agent of change is the heat shock protein known as HSP90. “It’s a very cool story in terms of the speed of evolution,” says Nicolas Rohner, lead author of the Science paper and a postdoctoral researcher in the lab of Harvard Medical School Genetics Professor Clifford Tabin. Rohner notes that at some point many thousands of years ago, a population of Astyanax mexicanus (a fish indigenous to northeastern Mexico) was swept from its hospitable river home into the unfriendly confines of underwater caves. Facing a dramatically different environment, the fish were forced to adapt. Living in near total darkness, the fish did away with their pigmentation, developed heightened sensory systems to detect changes in water pressure and the presence of prey and, perhaps most strikingly, they lost their eyes. Although seemingly counterintuitive, the loss of eyes is thought to be an “adaptive” or beneficial trait, as the maintenance of a complex but now useless organ would come at a high metabolic cost. Thus, the fish could reallocate their finite physiological resources to biological functions more helpful in the cave setting. Eye loss in these fish is considered to be a demonstration of an evolutionary concept known as “standing genetic variation,” which argues that pools of genetic mutations—some potentially helpful—exist in a given population but are normally kept silent. The manifestations of these mutations, that is, their impact on observable phenotypes, don’t emerge until the population encounters stressful conditions. But what exactly keeps those mutations at bay? Enter Whitehead Member Susan Lindquist, whose research has shown that HSP90 silences such genetic variation in a variety of organisms, from fruit flies, to yeast, to plants. Lindquist’s work found that the normally robust cellular reservoir of HSP90 becomes depleted during periods of physiological stress.… More:
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