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17 Molecular Mechanisms of Aging: Insights from Budding Yeast

Su-Ju Lin, David Sinclair


Until the late 1980s, the prevailing view among researchers was that life span of any organism, even yeast, could not be regulated, let alone by just a few genes. The view was based on the fact that aging is an incredibly complex process that is affected by thousands of genes. Then, in just a few years, genetic studies in model organisms such as Saccharomyces cerevisiae and Caenorhabditis elegans uncovered numerous single-gene mutations that extend life span (Jazwinski et al. 1993; Kenyon et al. 1993; Kennedy et al. 1995). What had researchers overlooked prior to 1990? The major oversight appears to have been the failure to foresee that organisms have evolved to promote their survival, and hence longevity, during times of adversity. Longevity regulation, as it has come to be known, is now thought of as a highly adaptive biological trait that is conserved all the way from yeast to mammals (Kirkwood and Holliday 1979; Kenyon 2001).

When Andrew Barton first proposed in 1950 that S. cerevisiae might serve as a model for aging, he was met with considerable skepticism (Barton 1950). It was difficult for most researchers to accept that a simple unicellular organism could provide any information about aging. But we have since learned never to underestimate a fungus. Today, S. cerevisiae is one of the most highly utilized models for aging, and dozens of longevity genes have been identified. Translating these findings to mammals is one of the major challenges for researchers during the next decade.


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