MSN2 and MSN4 link calorie restriction and TOR to sirtuin-mediated lifespan extension in Saccharomyces cerevisiae.
Identifieur interne : 001714 ( Main/Exploration ); précédent : 001713; suivant : 001715MSN2 and MSN4 link calorie restriction and TOR to sirtuin-mediated lifespan extension in Saccharomyces cerevisiae.
Auteurs : Oliver Medvedik [États-Unis] ; Dudley W. Lamming ; Keyman D. Kim ; David A. SinclairSource :
- PLoS biology [ 1545-7885 ] ; 2007.
Descripteurs français
- KwdFr :
- ADN ribosomique (génétique), Espérance de vie (MeSH), Facteurs de transcription (physiologie), Protein-Serine-Threonine Kinases (MeSH), Protéines de Saccharomyces cerevisiae (physiologie), Protéines de liaison à l'ADN (physiologie), Restriction calorique (MeSH), Saccharomyces cerevisiae (physiologie), Transduction du signal (MeSH).
- MESH :
English descriptors
- KwdEn :
- Caloric Restriction (MeSH), DNA, Ribosomal (genetics), DNA-Binding Proteins (physiology), Life Expectancy (MeSH), Protein-Serine-Threonine Kinases (MeSH), Saccharomyces cerevisiae (physiology), Saccharomyces cerevisiae Proteins (physiology), Signal Transduction (MeSH), Transcription Factors (physiology).
- MESH :
- chemical , genetics : DNA, Ribosomal.
- chemical , physiology : DNA-Binding Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- physiology : Saccharomyces cerevisiae.
- Caloric Restriction, Life Expectancy, Protein-Serine-Threonine Kinases, Signal Transduction.
Abstract
Calorie restriction (CR) robustly extends the lifespan of numerous species. In the yeast Saccharomyces cerevisiae, CR has been proposed to extend lifespan by boosting the activity of sirtuin deacetylases, thereby suppressing the formation of toxic repetitive ribosomal DNA (rDNA) circles. An alternative theory is that CR works by suppressing the TOR (target of rapamycin) signaling pathway, which extends lifespan via mechanisms that are unknown but thought to be independent of sirtuins. Here we show that TOR inhibition extends lifespan by the same mechanism as CR: by increasing Sir2p activity and stabilizing the rDNA locus. Further, we show that rDNA stabilization and lifespan extension by both CR and TOR signaling is due to the relocalization of the transcription factors Msn2p and Msn4p from the cytoplasm to the nucleus, where they increase expression of the nicotinamidase gene PNC1. These findings suggest that TOR and sirtuins may be part of the same longevity pathway in higher organisms, and that they may promote genomic stability during aging.
DOI: 10.1371/journal.pbio.0050261
PubMed: 17914901
PubMed Central: PMC1994990
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Glenn Laboratories for the Biological Mechanisms of Aging, Department of Pathology, Harvard Medical School, Boston, Massachusetts, United States of America.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Paul F. Glenn Laboratories for the Biological Mechanisms of Aging, Department of Pathology, Harvard Medical School, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Lamming, Dudley W" sort="Lamming, Dudley W" uniqKey="Lamming D" first="Dudley W" last="Lamming">Dudley W. Lamming</name></author><author><name sortKey="Kim, Keyman D" sort="Kim, Keyman D" uniqKey="Kim K" first="Keyman D" last="Kim">Keyman D. Kim</name></author><author><name sortKey="Sinclair, David A" sort="Sinclair, David A" uniqKey="Sinclair D" first="David A" last="Sinclair">David A. Sinclair</name></author></analytic><series><title level="j">PLoS biology</title><idno type="eISSN">1545-7885</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Caloric Restriction (MeSH)</term><term>DNA, Ribosomal (genetics)</term><term>DNA-Binding Proteins (physiology)</term><term>Life Expectancy (MeSH)</term><term>Protein-Serine-Threonine Kinases (MeSH)</term><term>Saccharomyces cerevisiae (physiology)</term><term>Saccharomyces cerevisiae Proteins (physiology)</term><term>Signal Transduction (MeSH)</term><term>Transcription Factors (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN ribosomique (génétique)</term><term>Espérance de vie (MeSH)</term><term>Facteurs de transcription (physiologie)</term><term>Protein-Serine-Threonine Kinases (MeSH)</term><term>Protéines de Saccharomyces cerevisiae (physiologie)</term><term>Protéines de liaison à l'ADN (physiologie)</term><term>Restriction calorique (MeSH)</term><term>Saccharomyces cerevisiae (physiologie)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA, Ribosomal</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>DNA-Binding Proteins</term><term>Saccharomyces cerevisiae Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ADN ribosomique</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Facteurs de transcription</term><term>Protéines de Saccharomyces cerevisiae</term><term>Protéines de liaison à l'ADN</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Caloric Restriction</term><term>Life Expectancy</term><term>Protein-Serine-Threonine Kinases</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Espérance de vie</term><term>Protein-Serine-Threonine Kinases</term><term>Restriction calorique</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Calorie restriction (CR) robustly extends the lifespan of numerous species. In the yeast Saccharomyces cerevisiae, CR has been proposed to extend lifespan by boosting the activity of sirtuin deacetylases, thereby suppressing the formation of toxic repetitive ribosomal DNA (rDNA) circles. An alternative theory is that CR works by suppressing the TOR (target of rapamycin) signaling pathway, which extends lifespan via mechanisms that are unknown but thought to be independent of sirtuins. Here we show that TOR inhibition extends lifespan by the same mechanism as CR: by increasing Sir2p activity and stabilizing the rDNA locus. Further, we show that rDNA stabilization and lifespan extension by both CR and TOR signaling is due to the relocalization of the transcription factors Msn2p and Msn4p from the cytoplasm to the nucleus, where they increase expression of the nicotinamidase gene PNC1. These findings suggest that TOR and sirtuins may be part of the same longevity pathway in higher organisms, and that they may promote genomic stability during aging.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17914901</PMID><DateCompleted><Year>2008</Year><Month>01</Month><Day>16</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1545-7885</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><Issue>10</Issue><PubDate><Year>2007</Year><Month>Oct</Month><Day>02</Day></PubDate></JournalIssue><Title>PLoS biology</Title><ISOAbbreviation>PLoS Biol</ISOAbbreviation></Journal><ArticleTitle>MSN2 and MSN4 link calorie restriction and TOR to sirtuin-mediated lifespan extension in Saccharomyces cerevisiae.</ArticleTitle><Pagination><MedlinePgn>e261</MedlinePgn></Pagination><Abstract><AbstractText>Calorie restriction (CR) robustly extends the lifespan of numerous species. In the yeast Saccharomyces cerevisiae, CR has been proposed to extend lifespan by boosting the activity of sirtuin deacetylases, thereby suppressing the formation of toxic repetitive ribosomal DNA (rDNA) circles. An alternative theory is that CR works by suppressing the TOR (target of rapamycin) signaling pathway, which extends lifespan via mechanisms that are unknown but thought to be independent of sirtuins. Here we show that TOR inhibition extends lifespan by the same mechanism as CR: by increasing Sir2p activity and stabilizing the rDNA locus. Further, we show that rDNA stabilization and lifespan extension by both CR and TOR signaling is due to the relocalization of the transcription factors Msn2p and Msn4p from the cytoplasm to the nucleus, where they increase expression of the nicotinamidase gene PNC1. These findings suggest that TOR and sirtuins may be part of the same longevity pathway in higher organisms, and that they may promote genomic stability during aging.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Medvedik</LastName><ForeName>Oliver</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Paul F. 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Kim</name><name sortKey="Lamming, Dudley W" sort="Lamming, Dudley W" uniqKey="Lamming D" first="Dudley W" last="Lamming">Dudley W. Lamming</name><name sortKey="Sinclair, David A" sort="Sinclair, David A" uniqKey="Sinclair D" first="David A" last="Sinclair">David A. Sinclair</name></noCountry><country name="États-Unis"><region name="Massachusetts"><name sortKey="Medvedik, Oliver" sort="Medvedik, Oliver" uniqKey="Medvedik O" first="Oliver" last="Medvedik">Oliver Medvedik</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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