{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Padilla CM"],"funding":["U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences","U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS)","NIGMS NIH HHS"],"pagination":["220"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12779999"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(1)"],"pubmed_abstract":["The Target of Rapamycin kinase Complex I (TORC1) is a central hub in the cell growth and metabolic control network of eukaryotes. How its upstream regulators cooperate to tune signaling across environmental conditions remains unclear. Here, we combine phosphoproteomics, TORC1 activity assays, and targeted genetic perturbations to dissect TORC1 regulation in Saccharomyces cerevisiae during transitions from a high-quality nitrogen source (glutamine) to a low-quality nitrogen source (proline), and on to complete nitrogen starvation. In proline medium, Ait1 and Gcn2 attenuate TORC1 activity, establishing a partially inhibited \"Low Nitrogen Adaptive\" state marked by extensive metabolic reprogramming without growth arrest. In contrast, during nitrogen starvation, SEAC, Ait1, and Gcn2 cooperate t"],"journal":["Nature communications"],"pubmed_title":["Multilayered regulation of TORC1 signaling by Ait1, Gcn2, and SEAC/GATOR during nitrogen limitation and starvation."],"pmcid":["PMC12779999"],"funding_grant_id":["R01 GM097329","T32 GM139779","R01GM097329","T32 GM136536","T32GM136536","R35 GM158300"],"pubmed_authors":["Padilla CM","Lipinski AA","Langlais PR","Lim J","Capaldi AP"],"additional_accession":[]},"is_claimable":false,"name":"Multilayered regulation of TORC1 signaling by Ait1, Gcn2, and SEAC/GATOR during nitrogen limitation and starvation.","description":"The Target of Rapamycin kinase Complex I (TORC1) is a central hub in the cell growth and metabolic control network of eukaryotes. How its upstream regulators cooperate to tune signaling across environmental conditions remains unclear. Here, we combine phosphoproteomics, TORC1 activity assays, and targeted genetic perturbations to dissect TORC1 regulation in Saccharomyces cerevisiae during transitions from a high-quality nitrogen source (glutamine) to a low-quality nitrogen source (proline), and on to complete nitrogen starvation. In proline medium, Ait1 and Gcn2 attenuate TORC1 activity, establishing a partially inhibited \"Low Nitrogen Adaptive\" state marked by extensive metabolic reprogramming without growth arrest. In contrast, during nitrogen starvation, SEAC, Ait1, and Gcn2 cooperate t","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-06T12:52:50.032Z","creation":"2026-05-30T03:11:19.161Z"},"accession":"S-EPMC12779999","cross_references":{"pubmed":["41318596"],"doi":["10.1038/s41467-025-66907-1"]}}