RapamycinFungusV1, Main, Exploration, bibRecord, 001563

Yeast life span extension by depletion of 60s ribosomal subunits is mediated by Gcn4.

Identifieur interne : 001563 ( Main/Exploration ); précédent : 001562; suivant : 001564

Yeast life span extension by depletion of 60s ribosomal subunits is mediated by Gcn4.

Auteurs : Kristan K. Steffen [États-Unis] ; Vivian L. Mackay ; Emily O. Kerr ; Mitsuhiro Tsuchiya ; Di Hu ; Lindsay A. Fox ; Nick Dang ; Elijah D. Johnston ; Jonathan A. Oakes ; Bie N. Tchao ; Diana N. Pak ; Stanley Fields ; Brian K. Kennedy ; Matt Kaeberlein

Source :

Cell [ 1097-4172 ] ; 2008.

RBID : pubmed:18423200

Descripteurs français

English descriptors

KwdEn :
- Basic-Leucine Zipper Transcription Factors (MeSH), DNA-Binding Proteins (physiology), Gene Deletion (MeSH), Histone Deacetylases (physiology), Ribosomal Proteins (physiology), Ribosome Subunits, Large, Eukaryotic (physiology), Saccharomyces cerevisiae (physiology), Saccharomyces cerevisiae Proteins (physiology), Silent Information Regulator Proteins, Saccharomyces cerevisiae (physiology), Sirtuin 2 (MeSH), Sirtuins (physiology), Transcription Factors (physiology).
MESH :
- chemical , physiology : DNA-Binding Proteins, Histone Deacetylases, Ribosomal Proteins, Saccharomyces cerevisiae Proteins, Silent Information Regulator Proteins, Saccharomyces cerevisiae, Sirtuins, Transcription Factors.
- chemical : Basic-Leucine Zipper Transcription Factors, Sirtuin 2.
- physiology : Ribosome Subunits, Large, Eukaryotic, Saccharomyces cerevisiae.
- Gene Deletion.

Abstract

In nearly every organism studied, reduced caloric intake extends life span. In yeast, span extension from dietary restriction is thought to be mediated by the highly conserved, nutrient-responsive target of rapamycin (TOR), protein kinase A (PKA), and Sch9 kinases. These kinases coordinately regulate various cellular processes including stress responses, protein turnover, cell growth, and ribosome biogenesis. Here we show that a specific reduction of 60S ribosomal subunit levels slows aging in yeast. Deletion of genes encoding 60S subunit proteins or processing factors or treatment with a small molecule, which all inhibit 60S subunit biogenesis, are each sufficient to significantly increase replicative life span. One mechanism by which reduced 60S subunit levels leads to life span extension is through induction of Gcn4, a nutrient-responsive transcription factor. Genetic epistasis analyses suggest that dietary restriction, reduced 60S subunit abundance, and Gcn4 activation extend yeast life span by similar mechanisms.

DOI: 10.1016/j.cell.2008.02.037
PubMed: 18423200
PubMed Central: PMC2749658

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<front><div type="abstract" xml:lang="en">In nearly every organism studied, reduced caloric intake extends life span. In yeast, span extension from dietary restriction is thought to be mediated by the highly conserved, nutrient-responsive target of rapamycin (TOR), protein kinase A (PKA), and Sch9 kinases. These kinases coordinately regulate various cellular processes including stress responses, protein turnover, cell growth, and ribosome biogenesis. Here we show that a specific reduction of 60S ribosomal subunit levels slows aging in yeast. Deletion of genes encoding 60S subunit proteins or processing factors or treatment with a small molecule, which all inhibit 60S subunit biogenesis, are each sufficient to significantly increase replicative life span. One mechanism by which reduced 60S subunit levels leads to life span extension is through induction of Gcn4, a nutrient-responsive transcription factor. Genetic epistasis analyses suggest that dietary restriction, reduced 60S subunit abundance, and Gcn4 activation extend yeast life span by similar mechanisms.</div>
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<Abstract><AbstractText>In nearly every organism studied, reduced caloric intake extends life span. In yeast, span extension from dietary restriction is thought to be mediated by the highly conserved, nutrient-responsive target of rapamycin (TOR), protein kinase A (PKA), and Sch9 kinases. These kinases coordinately regulate various cellular processes including stress responses, protein turnover, cell growth, and ribosome biogenesis. Here we show that a specific reduction of 60S ribosomal subunit levels slows aging in yeast. Deletion of genes encoding 60S subunit proteins or processing factors or treatment with a small molecule, which all inhibit 60S subunit biogenesis, are each sufficient to significantly increase replicative life span. One mechanism by which reduced 60S subunit levels leads to life span extension is through induction of Gcn4, a nutrient-responsive transcription factor. Genetic epistasis analyses suggest that dietary restriction, reduced 60S subunit abundance, and Gcn4 activation extend yeast life span by similar mechanisms.</AbstractText>
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	Serveur d'exploration sur la rapamycine et les champignons
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Yeast life span extension by depletion of 60s ribosomal subunits is mediated by Gcn4.

Yeast life span extension by depletion of 60s ribosomal subunits is mediated by Gcn4.

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