Endolysosomal membrane trafficking complexes drive nutrient-dependent TORC1 signaling to control cell growth in Saccharomyces cerevisiae.
Identifieur interne : 000E90 ( Main/Exploration ); précédent : 000E89; suivant : 000E91Endolysosomal membrane trafficking complexes drive nutrient-dependent TORC1 signaling to control cell growth in Saccharomyces cerevisiae.
Auteurs : Joanne M. Kingsbury [États-Unis] ; Neelam D. Sen ; Tatsuya Maeda ; Joseph Heitman ; Maria E. CardenasSource :
- Genetics [ 1943-2631 ] ; 2014.
Descripteurs français
- KwdFr :
- Acides aminés (métabolisme), Antifongiques (pharmacologie), Facteurs de transcription (génétique), Facteurs de transcription (métabolisme), Mutation (MeSH), Prolifération cellulaire (effets des médicaments et des substances chimiques), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines du transport vésiculaire (génétique), Protéines du transport vésiculaire (métabolisme), Saccharomyces cerevisiae (croissance et développement), Saccharomyces cerevisiae (cytologie), Saccharomyces cerevisiae (métabolisme), Sirolimus (pharmacologie), Transduction du signal (effets des médicaments et des substances chimiques).
- MESH :
- croissance et développement : Saccharomyces cerevisiae.
- cytologie : Saccharomyces cerevisiae.
- effets des médicaments et des substances chimiques : Prolifération cellulaire, Transduction du signal.
- génétique : Facteurs de transcription, Protéines de Saccharomyces cerevisiae, Protéines du transport vésiculaire.
- métabolisme : Acides aminés, Facteurs de transcription, Protéines de Saccharomyces cerevisiae, Protéines du transport vésiculaire, Saccharomyces cerevisiae.
- pharmacologie : Antifongiques, Sirolimus.
- Mutation.
English descriptors
- KwdEn :
- Amino Acids (metabolism), Antifungal Agents (pharmacology), Cell Proliferation (drug effects), Mutation (MeSH), Saccharomyces cerevisiae (cytology), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (drug effects), Sirolimus (pharmacology), Transcription Factors (genetics), Transcription Factors (metabolism), Vesicular Transport Proteins (genetics), Vesicular Transport Proteins (metabolism).
- MESH :
- chemical , genetics : Saccharomyces cerevisiae Proteins, Transcription Factors, Vesicular Transport Proteins.
- chemical , metabolism : Amino Acids, Saccharomyces cerevisiae Proteins, Transcription Factors, Vesicular Transport Proteins.
- chemical , pharmacology : Antifungal Agents, Sirolimus.
- cytology : Saccharomyces cerevisiae.
- drug effects : Cell Proliferation, Signal Transduction.
- growth & development : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- Mutation.
Abstract
The rapamycin-sensitive and endomembrane-associated TORC1 pathway controls cell growth in response to nutrients in eukaryotes. Mutations in class C Vps (Vps-C) complexes are synthetically lethal with tor1 mutations and confer rapamycin hypersensitivity in Saccharomyces cerevisiae, suggesting a role for these complexes in TORC1 signaling. Vps-C complexes are required for vesicular trafficking and fusion and comprise four distinct complexes: HOPS and CORVET and their minor intermediaries (i)-CORVET and i-HOPS. We show that at least one Vps-C complex is required to promote TORC1 activity, with the HOPS complex having the greatest input. The vps-c mutants fail to recover from rapamycin-induced growth arrest and show low levels of TORC1 activity. TORC1 promotes cell growth via Sch9, a p70(S6) kinase ortholog. Constitutively active SCH9 or hyperactive TOR1 alleles restored rapamycin recovery and TORC1 activity of vps-c mutants, supporting a role for the Vps-C complexes upstream of TORC1. The EGO GTPase complex Exit from G0 Complex (EGOC) and its homologous Rag-GTPase complex convey amino acid signals to TORC1 in yeast and mammals, respectively. Expression of the activated EGOC GTPase subunits Gtr1(GTP) and Gtr2(GDP) partially suppressed vps-c mutant rapamycin recovery defects, and this suppression was enhanced by increased amino acid concentrations. Moreover, vps-c mutations disrupted EGOC-TORC1 interactions. TORC1 defects were more severe for vps-c mutants than those observed in EGOC mutants. Taken together, our results support a model in which distinct endolysosomal trafficking Vps-C complexes promote rapamycin-sensitive TORC1 activity via multiple inputs, one of which involves maintenance of amino acid homeostasis that is sensed and transmitted to TORC1 via interactions with EGOC.
DOI: 10.1534/genetics.114.161646
PubMed: 24514902
PubMed Central: PMC3982701
Affiliations:
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Mutations in class C Vps (Vps-C) complexes are synthetically lethal with tor1 mutations and confer rapamycin hypersensitivity in Saccharomyces cerevisiae, suggesting a role for these complexes in TORC1 signaling. Vps-C complexes are required for vesicular trafficking and fusion and comprise four distinct complexes: HOPS and CORVET and their minor intermediaries (i)-CORVET and i-HOPS. We show that at least one Vps-C complex is required to promote TORC1 activity, with the HOPS complex having the greatest input. The vps-c mutants fail to recover from rapamycin-induced growth arrest and show low levels of TORC1 activity. TORC1 promotes cell growth via Sch9, a p70(S6) kinase ortholog. Constitutively active SCH9 or hyperactive TOR1 alleles restored rapamycin recovery and TORC1 activity of vps-c mutants, supporting a role for the Vps-C complexes upstream of TORC1. The EGO GTPase complex Exit from G0 Complex (EGOC) and its homologous Rag-GTPase complex convey amino acid signals to TORC1 in yeast and mammals, respectively. Expression of the activated EGOC GTPase subunits Gtr1(GTP) and Gtr2(GDP) partially suppressed vps-c mutant rapamycin recovery defects, and this suppression was enhanced by increased amino acid concentrations. Moreover, vps-c mutations disrupted EGOC-TORC1 interactions. TORC1 defects were more severe for vps-c mutants than those observed in EGOC mutants. Taken together, our results support a model in which distinct endolysosomal trafficking Vps-C complexes promote rapamycin-sensitive TORC1 activity via multiple inputs, one of which involves maintenance of amino acid homeostasis that is sensed and transmitted to TORC1 via interactions with EGOC.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24514902</PMID><DateCompleted><Year>2015</Year><Month>02</Month><Day>04</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1943-2631</ISSN><JournalIssue CitedMedium="Internet"><Volume>196</Volume><Issue>4</Issue><PubDate><Year>2014</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Genetics</Title><ISOAbbreviation>Genetics</ISOAbbreviation></Journal><ArticleTitle>Endolysosomal membrane trafficking complexes drive nutrient-dependent TORC1 signaling to control cell growth in Saccharomyces cerevisiae.</ArticleTitle><Pagination><MedlinePgn>1077-89</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1534/genetics.114.161646</ELocationID><Abstract><AbstractText>The rapamycin-sensitive and endomembrane-associated TORC1 pathway controls cell growth in response to nutrients in eukaryotes. Mutations in class C Vps (Vps-C) complexes are synthetically lethal with tor1 mutations and confer rapamycin hypersensitivity in Saccharomyces cerevisiae, suggesting a role for these complexes in TORC1 signaling. Vps-C complexes are required for vesicular trafficking and fusion and comprise four distinct complexes: HOPS and CORVET and their minor intermediaries (i)-CORVET and i-HOPS. We show that at least one Vps-C complex is required to promote TORC1 activity, with the HOPS complex having the greatest input. The vps-c mutants fail to recover from rapamycin-induced growth arrest and show low levels of TORC1 activity. TORC1 promotes cell growth via Sch9, a p70(S6) kinase ortholog. Constitutively active SCH9 or hyperactive TOR1 alleles restored rapamycin recovery and TORC1 activity of vps-c mutants, supporting a role for the Vps-C complexes upstream of TORC1. The EGO GTPase complex Exit from G0 Complex (EGOC) and its homologous Rag-GTPase complex convey amino acid signals to TORC1 in yeast and mammals, respectively. Expression of the activated EGOC GTPase subunits Gtr1(GTP) and Gtr2(GDP) partially suppressed vps-c mutant rapamycin recovery defects, and this suppression was enhanced by increased amino acid concentrations. Moreover, vps-c mutations disrupted EGOC-TORC1 interactions. TORC1 defects were more severe for vps-c mutants than those observed in EGOC mutants. Taken together, our results support a model in which distinct endolysosomal trafficking Vps-C complexes promote rapamycin-sensitive TORC1 activity via multiple inputs, one of which involves maintenance of amino acid homeostasis that is sensed and transmitted to TORC1 via interactions with EGOC.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kingsbury</LastName><ForeName>Joanne M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sen</LastName><ForeName>Neelam D</ForeName><Initials>ND</Initials></Author><Author ValidYN="Y"><LastName>Maeda</LastName><ForeName>Tatsuya</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Heitman</LastName><ForeName>Joseph</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Cardenas</LastName><ForeName>Maria E</ForeName><Initials>ME</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA154499</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA154499</GrantID><Acronym>CA</Acronym><Agency>NCI 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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>02</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Genetics</MedlineTA><NlmUniqueID>0374636</NlmUniqueID><ISSNLinking>0016-6731</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000596">Amino 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MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000935" MajorTopicYN="N">Antifungal Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D033921" MajorTopicYN="N">Vesicular Transport Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">HOPS</Keyword><Keyword MajorTopicYN="N">TORC1</Keyword><Keyword MajorTopicYN="N">amino acid homeostasis</Keyword><Keyword MajorTopicYN="N">class C Vps complex</Keyword><Keyword MajorTopicYN="N">rapamycin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>2</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>2</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24514902</ArticleId><ArticleId IdType="pii">genetics.114.161646</ArticleId><ArticleId 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Cardenas</name><name sortKey="Heitman, Joseph" sort="Heitman, Joseph" uniqKey="Heitman J" first="Joseph" last="Heitman">Joseph Heitman</name><name sortKey="Maeda, Tatsuya" sort="Maeda, Tatsuya" uniqKey="Maeda T" first="Tatsuya" last="Maeda">Tatsuya Maeda</name><name sortKey="Sen, Neelam D" sort="Sen, Neelam D" uniqKey="Sen N" first="Neelam D" last="Sen">Neelam D. Sen</name></noCountry><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Kingsbury, Joanne M" sort="Kingsbury, Joanne M" uniqKey="Kingsbury J" first="Joanne M" last="Kingsbury">Joanne M. Kingsbury</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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