ArticleeLife2023
Snf1/AMPK fine-tunes TORC1 signaling in response to glucose starvation.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it.
- An AI-Ready Phosphorylation Meta-Analysis forJournal of proteome research · 2026Pooled it
- Proteomic investigation of signaling dynamics: from static maps to network rewiring.Bioscience reports · 2026Review
- SIRT1 Exon 2-Encoded IDR Gates CREB-Dependent Transcriptional Timing During Fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Transcriptional Reprogramming of Lifespan-Associated Genes in Yeast Lacking TOR1.Biochemical genetics · 2026Article
- SNF1/AMPK controls its own localization by phosphorylating its activating kinase Sak1.iScience · 2026Article
- Protocol to study direct (de)phosphorylation events on a proteome-wide scale using on-bead in vitro enzyme assays.STAR protocols · 2026Article
- Experimental evolution of cellular miniaturization reveals a putative mechanism for cell size evolution.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Anhydrobiosis as a Model of Aging and Longevity: The Role of Autophagy and Metabolism in Yeast Cells.Microbial ecology · 2026Review
- Molecular frontiers of fungal autophagy: from molecular mechanisms to potential targets for antifungal drug discovery.World journal of microbiology & biotechnology · 2026Review
- Time-resolved functional genomics using deep learning reveals global hierarchical control of autophagy.Nature cell biology · 2026Article
- Ecological History Shapes Transcriptome Variation in QuiescentBiomolecules · 2025Article
- The small GTPase Rho5-Yet another player in yeast glucose signaling.PLoS genetics · 2025Article
- Possible regulatory network and associated pathways governing the expression of ADH2 in Saccharomyces cerevisiae.Current genetics · 2025Review
- Nitrogen limitation causes a seismic shift in redox state and phosphorylation of proteins implicated in carbon flux and lipidome remodeling in Rhodotorula toruloides.Biotechnology for biofuels and bioproducts · 2025Article
- Valproate independently activates Snf1, inhibits TORC1, and induces repression of INO1 transcription by increasing nuclear localization of Opi1.Scientific reports · 2025Article
- Regulatory dynamics of Sch9 in response to cytosolic acidification: From spatial reconfiguration to cellular adaptation to stresses.iScience · 2025Article
- Identification and characterization of yeast SNF1 kinase homologs inFrontiers in molecular biosciences · 2025Article
- Translation regulation in response to stress.The FEBS journal · 2024Review
- TORC1 Regulates Thermotolerance via Modulating Metabolic Rate and Antioxidant Capacity in ScallopAntioxidants (Basel, Switzerland) · 2024Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AMP-activated protein kinase (AMPK) and the target of rapamycin complex 1 (TORC1) are central kinase modules of two opposing signaling pathways that control eukaryotic cell growth and metabolism in response to the availability of energy and nutrients. Accordingly, energy depletion activates AMPK to inhibit growth, while nutrients and high energy levels activate TORC1 to promote growth. Both in mammals and lower eukaryotes such as yeast, the AMPK and TORC1 pathways are wired to each other at different levels, which ensures homeostatic control of growth and metabolism. In this context, a previous study (Hughes Hallett et al., 2015) reported that AMPK in yeast, that is Snf1, prevents the transient TORC1 reactivation during the early phase following acute glucose starvation, but the underlying mechanism has remained elusive. Using a combination of unbiased mass spectrometry (MS)-based phosphoproteomics, genetic, biochemical, and physiological experiments, we show here that Snf1 temporally maintains TORC1 inactive in glucose-starved cells primarily through the TORC1-regulatory protein Pib2. Our data, therefore, extend the function of Pib2 to a hub that integrates both glucose and, as reported earlier, glutamine signals to control TORC1. We further demonstrate that Snf1 phosphorylates the TORC1 effector kinase Sch9 within its N-terminal region and thereby antagonizes the phosphorylation of a C-terminal TORC1-target residue within Sch9 itself that is critical for its activity. The consequences of Snf1-mediated phosphorylation of Pib2 and Sch9 are physiologically additive and sufficient to explain the role of Snf1 in short-term inhibition of TORC1 in acutely glucose-starved cells.
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