Conclusion

As with other model organisms, the ultimate utility of yeast as a model for human aging has yet to be determined. Thus far, at least six genes and one environmental intervention (calorie restriction) have been found to increase life span in yeast and similarly impact longevity in one or more multicellular models of aging (Figure 18.2). Although it remains to be seen whether these potential conserved determinants of longevity are affecting aging through a similar mechanism in different organisms, there is reason for optimism that this is, indeed, the case. In particular, the recent findings that highly conserved nutrient responsive kinase pathways regulate aging in both dividing and nondividing yeast cells through divergent downstream components suggest a plausible mechanism by which CR might slow aging in both mitotic and postmitotic cell types of multicellular eukaryotes. Dissecting the genetic and molecular components of these nutrient responsive, longevity-determining pathways in yeast will provide direction for further study in complex systems.

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