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

DOI Web Site 被引用文献21件
  • Matt Kaeberlein
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • R. Wilson Powers
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • Kristan K. Steffen
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • Eric A. Westman
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • Di Hu
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • Nick Dang
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • Emily O. Kerr
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • Kathryn T. Kirkland
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • Stanley Fields
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.
  • Brian K. Kennedy
    Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA.

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<jats:p> Calorie restriction increases life span in many organisms, including the budding yeast <jats:italic>Saccharomyces cerevisiae</jats:italic> . 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 <jats:italic>tor1</jats:italic> D or <jats:italic>sch9</jats:italic> D cells failed to further increase life span and, like calorie restriction, deletion of either <jats:italic>SCH9</jats:italic> or <jats:italic>TOR1</jats:italic> 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. </jats:p>

収録刊行物

  • Science

    Science 310 (5751), 1193-1196, 2005-11-18

    American Association for the Advancement of Science (AAAS)

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