ArticleThe Journal of biological chemistry2017
Reciprocal Regulation of Target of Rapamycin Complex 1 and Potassium Accumulation.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Patterns of spontaneous and induced genomic alterations inApplied and environmental microbiology · 2025Article
- TORC pathway intersects with a calcium sensor kinase network to regulate potassium sensing inProceedings of the National Academy of Sciences of the United States of America · 2023Article
- The NPR/Hal family of protein kinases in yeasts: biological role, phylogeny and regulation under environmental challenges.Computational and structural biotechnology journal · 2022Review
- SARS-CoV2 Infection and the Importance of Potassium Balance.Frontiers in medicine · 2021Article
- Potassium starvation induces autophagy in yeast.The Journal of biological chemistry · 2020Article
- A Snf1-related nutrient-responsive kinase antagonizes endocytosis in yeast.PLoS genetics · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proper maintenance of potassium homeostasis is crucial for cell viability. Among the major determinants of potassium uptake in the model organism Saccharomyces cerevisiae are the Trk1 high affinity potassium transporter and the functionally redundant Hal4 (Sat4) and Hal5 protein kinases. These kinases are required for the plasma membrane accumulation of not only Trk1 but also several nutrient permeases. Here, we show that overexpression of the target of rapamycin complex 1 (TORC1) effector NPR1 improves hal4 hal5 growth defects by stabilizing nutrient permeases at the plasma membrane. We subsequently found that internal potassium levels and TORC1 activity are linked. Specifically, growth under limiting potassium alters the activities of Npr1 and another TORC1 effector kinase, Sch9; hal4 hal5 and trk1 trk2 mutants display hypersensitivity to rapamycin, and reciprocally, TORC1 inhibition reduces potassium accumulation. Our results demonstrate that in addition to carbon and nitrogen, TORC1 also responds to and regulates potassium fluxes.
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Registered trials
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