Calorie restriction seems to be the key to extend the lifespan of many species through Sir2 gene.
Researchers from Harvard Medical School, Boston and University of California, Davis, screened for genes that could increase yeast lifespan via Sir2 gene. According to the study published today in the advance online edition of Science, "Yeast and Drosophila lacking the Sir2 gene do not live longer when subjected to calorie restriction, suggesting that Sir2 underlies this lifespan extension." "However," they say, "there is increasing evidence that the situation is not so simple."
Advertisement"We think these new Sir2 genes are as important as any longevity genes discovered so far," said molecular biologist David Sinclair, director of the Paul F. Glenn Laboratories for Aging Research at Harvard Medical School and co-author of the new study. "There is a growing realization from the aging field that we might finally understand how to control certain aspects of the aging process and one day have drugs that can fight some of the disabilities the process causes."
There has been some controversy over the role of the gene Sir2 in the ability of caloric restriction to extend yeast lifespan and some recent work suggests that caloric-restriction-induced lifespan extension may not involve Sir2. The results also show that Hst2 is responsible for Sir2-independent lifespan extension by calorie restriction, and that it does so by suppressing ribosomal DNA recombination, which is the same mechanism by which Sir2 functions.
Sinclair's research group have earlier reported in the journal Nature about the first genetic link between environmental stresses and longer life. Triggered by low salt, heat, or extreme calorie restriction, a yeast "master longevity regulator" called PNC1 stimulated Sir2 activity. This work was done by Harvard graduate student Dudley Lamming, demonstrates that PNC1 regulates the whole SIR2 family of genes, suggesting that a human PNC1 gene might protect against diseases of aging such as cancer, heart disease and diabetes.
This work was supported by the National Institute on Aging, the Paul F. Glenn Foundation, and the Ellison Medical Foundation and further supported by fellowships and training grants from the American Federation for Aging Research and the National Eye Institute.
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