Abstract

In many organisms, nutrient sensing and caloric intake regulate aging and longevity, and in the budding yeast Saccharomyces cerevisiae , calorie restriction can increase replicative life span. Kaeberlein et al. (see the Perspective by Rine) analyzed 564 single-gene yeast deletion strains and identified 10 gene deletions that significantly increase replicative life span. Six of these encoded components of the highly conserved, nutrient-responsive TOR and Sch9 pathways. Calorie restriction of cells lacking TOR1 or Sch9 failed to increase life span further. Thus, it appears that TOR and Sch9 kinases are involved in a pathway through which excess caloric intake limits life span in yeast and, perhaps, higher eukaryotes. M. Kaeberlein, R. W. Powers, III, K. K. Steffen, E. A. Westman, D. Hu, N. Dang, E. O. Kerr, K. T. Kirkland, S. Fields, B. K. Kennedy, Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients. Science 310 , 1193-1196 (2005). [Abstract] [Full Text] J. Rine, Twists in the tale of the aging yeast. Science 310 , 1124-1125 (2005). [Summary] [Full Text]

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