Regulation of Yeast Replicative Life Span by TOR and Sch9 in Response to Nutrients

TLDR

Calorie restriction extends lifespan in many organisms, including budding yeast. The study proposes that TOR and Sch9 kinases mediate nutrient‑driven lifespan limitation in yeast. Deletion of 10 genes, six of which encode components of the TOR and Sch9 pathways, extends yeast replicative lifespan, and loss of TOR1 or SCH9 eliminates the additional benefit of calorie restriction, showing these kinases act independently of Sir2.

Abstract

Calorie restriction increases life span in many organisms, including the budding yeast Saccharomyces cerevisiae . From a large-scale analysis of 564 single-gene–deletion strains of yeast, we identified 10 gene deletions that increase replicative life span. Six of these correspond to genes encoding components of the nutrient-responsive TOR and Sch9 pathways. Calorie restriction of tor1 D or sch9 D cells failed to further increase life span and, like calorie restriction, deletion of either SCH9 or TOR1 increased life span independent of the Sir2 histone deacetylase. We propose that the TOR and Sch9 kinases define a primary conduit through which excess nutrient intake limits longevity in yeast.