Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients.
Identifieur interne : 001810 ( Main/Corpus ); précédent : 001809; suivant : 001811Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients.
Auteurs : Matt Kaeberlein ; R Wilson Powers ; Kristan K. Steffen ; Eric A. Westman ; Di Hu ; Nick Dang ; Emily O. Kerr ; Kathryn T. Kirkland ; Stanley Fields ; Brian K. KennedySource :
- Science (New York, N.Y.) [ 1095-9203 ] ; 2005.
English descriptors
- KwdEn :
- Cell Division (genetics), Cell Division (physiology), Gene Deletion (MeSH), Protein Kinases (metabolism), Protein-Serine-Threonine Kinases (MeSH), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae (physiology), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (physiology).
- MESH :
- chemical , genetics : Saccharomyces cerevisiae Proteins.
- chemical , metabolism : Protein Kinases.
- genetics : Cell Division, Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- physiology : Cell Division, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins.
- Gene Deletion, Protein-Serine-Threonine Kinases.
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.
DOI: 10.1126/science.1115535
PubMed: 16293764
Links to Exploration step
pubmed:16293764Le document en format XML
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<author><name sortKey="Kaeberlein, Matt" sort="Kaeberlein, Matt" uniqKey="Kaeberlein M" first="Matt" last="Kaeberlein">Matt Kaeberlein</name>
<affiliation><nlm:affiliation>Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA. kaeber@u.washington.edu</nlm:affiliation>
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<author><name sortKey="Powers, R Wilson" sort="Powers, R Wilson" uniqKey="Powers R" first="R Wilson" last="Powers">R Wilson Powers</name>
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<author><name sortKey="Steffen, Kristan K" sort="Steffen, Kristan K" uniqKey="Steffen K" first="Kristan K" last="Steffen">Kristan K. Steffen</name>
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<author><name sortKey="Westman, Eric A" sort="Westman, Eric A" uniqKey="Westman E" first="Eric A" last="Westman">Eric A. Westman</name>
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<author><name sortKey="Hu, Di" sort="Hu, Di" uniqKey="Hu D" first="Di" last="Hu">Di Hu</name>
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<author><name sortKey="Dang, Nick" sort="Dang, Nick" uniqKey="Dang N" first="Nick" last="Dang">Nick Dang</name>
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<author><name sortKey="Kerr, Emily O" sort="Kerr, Emily O" uniqKey="Kerr E" first="Emily O" last="Kerr">Emily O. Kerr</name>
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<author><name sortKey="Kirkland, Kathryn T" sort="Kirkland, Kathryn T" uniqKey="Kirkland K" first="Kathryn T" last="Kirkland">Kathryn T. Kirkland</name>
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<author><name sortKey="Fields, Stanley" sort="Fields, Stanley" uniqKey="Fields S" first="Stanley" last="Fields">Stanley Fields</name>
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<author><name sortKey="Kennedy, Brian K" sort="Kennedy, Brian K" uniqKey="Kennedy B" first="Brian K" last="Kennedy">Brian K. Kennedy</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients.</title>
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<author><name sortKey="Powers, R Wilson" sort="Powers, R Wilson" uniqKey="Powers R" first="R Wilson" last="Powers">R Wilson Powers</name>
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<author><name sortKey="Steffen, Kristan K" sort="Steffen, Kristan K" uniqKey="Steffen K" first="Kristan K" last="Steffen">Kristan K. Steffen</name>
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<author><name sortKey="Hu, Di" sort="Hu, Di" uniqKey="Hu D" first="Di" last="Hu">Di Hu</name>
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<term>Gene Deletion (MeSH)</term>
<term>Protein Kinases (metabolism)</term>
<term>Protein-Serine-Threonine Kinases (MeSH)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae (physiology)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (physiology)</term>
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<term>Saccharomyces cerevisiae</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Division</term>
<term>Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae Proteins</term>
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<front><div type="abstract" xml:lang="en">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.</div>
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<Abstract><AbstractText>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.</AbstractText>
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