Findings extend longevity research from yeast and worms to mammals
Researchers at Childrens Hospital Boston have discovered how two key cellular influences on lifespan work together, providing insights that may help reveal aging mechanisms in humans. The findings extend longevity research from yeast and worms into mammals, and suggest that longer life results, at least in part, from biochemical interactions that boost cells ability to resist environmental stresses while inhibiting them from committing suicide. The study appears in the February 19th Science Express, the online edition of the journal Science.
Previous studies in yeast and worms pinpointed a gene known as Sir2 as a key regulator of lifespan: deleting Sir2 limits lifespan, and extra copies lengthen it. Sir2 has a counterpart in mammals, but until now, very little was known about how it worked or what it had to do with aging. Working with mouse cells, researchers led by Anne Brunet, a postdoctoral fellow in neuroscience at Childrens Hospital who is now at Stanford University, discovered that Sir2 works by regulating a group of proteins known as FOXO transcription factors. FOXO proteins have also been linked with longevity; they control the expression of genes that regulate cell suicide, and also enable the cell to resist oxidative stress, or chemical stresses that can disrupt the cells DNA, or genetic blueprint.
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