Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients

Kaeberlein M; Kennedy BK et al. · 2005 · Science · Atlas ID KAE2005

A systematic screen of 564 yeast gene deletions found TOR and Sch9 pathway genes as the strongest lifespan-extending hits.

At a glance

Evidence tierC Animal in vivo
Study type4 - Animal Study
Model systemYeast (Saccharomyces cerevisiae)
JournalScience
Year2005
Peer reviewedYes
SourceDOI 10.1126/science.1115535 · PMID 16293764

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 tor1D or sch9D 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.

Extracted findings

InterventionGenetic (tor1Δ, sch9Δ) + caloric restriction
TargetTOR / Sch9
ModelYeast (S. cerevisiae)
EffectDeleting TOR or Sch9 extends yeast replicative lifespan, overlapping with the caloric-restriction effect

Related topics

mTORLongevity

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