Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients.
Identifieur interne : 001825 ( Main/Exploration ); précédent : 001824; suivant : 001826Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients.
Auteurs : Matt Kaeberlein [États-Unis] ; 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.
Descripteurs français
- KwdFr :
- Division cellulaire (génétique), Division cellulaire (physiologie), Délétion de gène (MeSH), Protein kinases (métabolisme), Protein-Serine-Threonine Kinases (MeSH), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (physiologie), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Saccharomyces cerevisiae (physiologie).
- MESH :
- génétique : Division cellulaire, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae.
- métabolisme : Protein kinases, Saccharomyces cerevisiae.
- physiologie : Division cellulaire, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae.
- Délétion de gène, Protein-Serine-Threonine Kinases.
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
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Kennedy</name></author></analytic><series><title level="j">Science (New York, N.Y.)</title><idno type="eISSN">1095-9203</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Division (genetics)</term><term>Cell Division (physiology)</term><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></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Division cellulaire (génétique)</term><term>Division cellulaire (physiologie)</term><term>Délétion de gène (MeSH)</term><term>Protein kinases (métabolisme)</term><term>Protein-Serine-Threonine Kinases (MeSH)</term><term>Protéines de Saccharomyces cerevisiae (génétique)</term><term>Protéines de Saccharomyces cerevisiae (physiologie)</term><term>Saccharomyces cerevisiae (génétique)</term><term>Saccharomyces cerevisiae (métabolisme)</term><term>Saccharomyces cerevisiae (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Saccharomyces cerevisiae Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Protein Kinases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Division</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Division cellulaire</term><term>Protéines de Saccharomyces cerevisiae</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protein kinases</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Division cellulaire</term><term>Protéines de Saccharomyces cerevisiae</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Division</term><term>Saccharomyces cerevisiae</term><term>Saccharomyces cerevisiae Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Gene Deletion</term><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Délétion de gène</term><term>Protein-Serine-Threonine Kinases</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16293764</PMID><DateCompleted><Year>2005</Year><Month>11</Month><Day>30</Day></DateCompleted><DateRevised><Year>2009</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1095-9203</ISSN><JournalIssue CitedMedium="Internet"><Volume>310</Volume><Issue>5751</Issue><PubDate><Year>2005</Year><Month>Nov</Month><Day>18</Day></PubDate></JournalIssue><Title>Science (New York, N.Y.)</Title><ISOAbbreviation>Science</ISOAbbreviation></Journal><ArticleTitle>Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients.</ArticleTitle><Pagination><MedlinePgn>1193-6</MedlinePgn></Pagination><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></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kaeberlein</LastName><ForeName>Matt</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Departments of Genome Sciences and Medicine, University of Washington, Seattle, WA 98195, USA. kaeber@u.washington.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Powers</LastName><ForeName>R Wilson</ForeName><Initials>RW</Initials><Suffix>3rd</Suffix></Author><Author ValidYN="Y"><LastName>Steffen</LastName><ForeName>Kristan K</ForeName><Initials>KK</Initials></Author><Author ValidYN="Y"><LastName>Westman</LastName><ForeName>Eric A</ForeName><Initials>EA</Initials></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Di</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Dang</LastName><ForeName>Nick</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Kerr</LastName><ForeName>Emily O</ForeName><Initials>EO</Initials></Author><Author ValidYN="Y"><LastName>Kirkland</LastName><ForeName>Kathryn T</ForeName><Initials>KT</Initials></Author><Author ValidYN="Y"><LastName>Fields</LastName><ForeName>Stanley</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Kennedy</LastName><ForeName>Brian K</ForeName><Initials>BK</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P30 AG013280</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType 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cerevisiae</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Science. 2005 Nov 18;310(5751):1124-5</RefSource><PMID Version="1">16293743</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D002455" MajorTopicYN="N">Cell Division</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011494" MajorTopicYN="N">Protein Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>11</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>12</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>11</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16293764</ArticleId><ArticleId IdType="pii">310/5751/1193</ArticleId><ArticleId IdType="doi">10.1126/science.1115535</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><noCountry><name sortKey="Dang, Nick" sort="Dang, Nick" uniqKey="Dang N" first="Nick" last="Dang">Nick Dang</name><name sortKey="Fields, Stanley" sort="Fields, Stanley" uniqKey="Fields S" first="Stanley" last="Fields">Stanley Fields</name><name sortKey="Hu, Di" sort="Hu, Di" uniqKey="Hu D" first="Di" last="Hu">Di Hu</name><name sortKey="Kennedy, Brian K" sort="Kennedy, Brian K" uniqKey="Kennedy B" first="Brian K" last="Kennedy">Brian K. Kennedy</name><name sortKey="Kerr, Emily O" sort="Kerr, Emily O" uniqKey="Kerr E" first="Emily O" last="Kerr">Emily O. Kerr</name><name sortKey="Kirkland, Kathryn T" sort="Kirkland, Kathryn T" uniqKey="Kirkland K" first="Kathryn T" last="Kirkland">Kathryn T. Kirkland</name><name sortKey="Powers, R Wilson" sort="Powers, R Wilson" uniqKey="Powers R" first="R Wilson" last="Powers">R Wilson Powers</name><name sortKey="Steffen, Kristan K" sort="Steffen, Kristan K" uniqKey="Steffen K" first="Kristan K" last="Steffen">Kristan K. Steffen</name><name sortKey="Westman, Eric A" sort="Westman, Eric A" uniqKey="Westman E" first="Eric A" last="Westman">Eric A. Westman</name></noCountry><country name="États-Unis"><region name="Washington (État)"><name sortKey="Kaeberlein, Matt" sort="Kaeberlein, Matt" uniqKey="Kaeberlein M" first="Matt" last="Kaeberlein">Matt Kaeberlein</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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