ArticleGenetics2014
Endolysosomal membrane trafficking complexes drive nutrient-dependent TORC1 signaling to control cell growth in Saccharomyces cerevisiae.
Article in Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- The yeast Mkt1/Pbp1 complex promotes adaptive responses to respiratory growth.The Journal of cell biology · 2025Article
- Cooperative Function of Atg8- and TORC1-Mediated Activities in Yeast.Yeast (Chichester, England) · 2025Article
- The GTPase activating protein Gyp7 regulates Rab7/Ypt7 activity on late endosomes.The Journal of cell biology · 2024Article
- Estragole Inhibits Growth and Aflatoxin Biosynthesis ofMicrobiology spectrum · 2023Article
- Human gasdermin D and MLKL disrupt mitochondria, endocytic traffic and TORC1 signalling in budding yeast.Open biology · 2023Article
- The nutrient-responsive CDK Pho85 primes the Sch9 kinase for its activation by TORC1.PLoS genetics · 2023Article
- The HOPS tethering complex is required to maintain signaling endosome identity and TORC1 activity.The Journal of cell biology · 2022Article
- Feedback regulation of TORC1 by its downstream effectors Npr1 and Par32.Molecular biology of the cell · 2018Article
- Ivy1 is a negative regulator of Gtr-dependent TORC1 activation.Journal of cell science · 2018Article
- The endosomal trafficking factors CORVET and ESCRT suppress plasma membrane residence of the renal outer medullary potassium channel (ROMK).The Journal of biological chemistry · 2018Article
- Vacuole-mediated selective regulation of TORC1-Sch9 signaling following oxidative stress.Molecular biology of the cell · 2018Article
- Overproduction of Sch9 leads to its aggregation and cell elongation in Saccharomyces cerevisiae.PloS one · 2018Article
- Pib2 and the EGO complex are both required for activation of TORC1.Journal of cell science · 2017Article
- The nutrient transceptor/PKA pathway functions independently of TOR and responds to leucine and Gcn2 in a TOR-independent manner.FEMS yeast research · 2017Article
- The Architecture of the Rag GTPase Signaling Network.Biomolecules · 2017Review
- Phosphate is the third nutrient monitored by TOR inProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Hygromycin B hypersensitive (hhy) mutants implicate an intact trans-Golgi and late endosome interface in efficient Tor1 vacuolar localization and TORC1 function.Current genetics · 2017Article
- The yeast protein kinase Sch9 adjusts V-ATPase assembly/disassembly to control pH homeostasis and longevity in response to glucose availability.PLoS genetics · 2017Article
- Conceptualizing Eukaryotic Metabolic Sensing and Signaling.Journal of the Indian Institute of Science · 2017Article
- Target of rapamycin signaling mediates vacuolar fragmentation.Current genetics · 2017Review
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.