| http://purl.uniprot.org/citations/24514902 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24514902 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.org/dc/terms/identifier | "doi:10.1534/genetics.114.161646"xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/author | "Heitman J."xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/author | "Maeda T."xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/author | "Cardenas M.E."xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/author | "Kingsbury J.M."xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/author | "Sen N.D."xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/name | "Genetics"xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/pages | "1077-1089"xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/title | "Endolysosomal membrane trafficking complexes drive nutrient-dependent TORC1 signaling to control cell growth in Saccharomyces cerevisiae."xsd:string |
| http://purl.uniprot.org/citations/24514902 | http://purl.uniprot.org/core/volume | "196"xsd:string |
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