ArticlePloS one2013
The AMPK family member Snf1 protects Saccharomyces cerevisiae cells upon glutathione oxidation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Advances inJournal of fungi (Basel, Switzerland) · 2023Review
- Review
- Conventional and emerging roles of the energy sensor Snf1/AMPK inMicrobial cell (Graz, Austria) · 2018Review
- Snf1 cooperates with the CWI MAPK pathway to mediate the degradation of Med13 following oxidative stress.Microbial cell (Graz, Austria) · 2018Article
- The yeast Aft2 transcription factor determines selenite toxicity by controlling the low affinity phosphate transport system.Scientific reports · 2016Article
- Coordinate responses to alkaline pH stress in budding yeast.Microbial cell (Graz, Austria) · 2015Review
- Yeast as a model system to study metabolic impact of selenium compounds.Microbial cell (Graz, Austria) · 2015Review
- Nutrient sensing and signaling in the yeast Saccharomyces cerevisiae.FEMS microbiology reviews · 2014Review
- Crosstalk between SNF1 pathway and the peroxisome-mediated lipid metabolism in Magnaporthe oryzae.PloS one · 2014Article
- Combination of fenretinide and selenite inhibits proliferation and induces apoptosis in ovarian cancer cells.International journal of molecular sciences · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AMPK/Snf1 kinase has a central role in carbon metabolism homeostasis in Saccharomyces cerevisiae. In this study, we show that Snf1 activity, which requires phosphorylation of the Thr210 residue, is needed for protection against selenite toxicity. Such protection involves the Elm1 kinase, which acts upstream of Snf1 to activate it. Basal Snf1 activity is sufficient for the defense against selenite, although Snf1 Thr210 phosphorylation levels become increased at advanced treatment times, probably by inhibition of the Snf1 dephosphorylation function of the Reg1 phosphatase. Contrary to glucose deprivation, Snf1 remains cytosolic during selenite treatment, and the protective function of the kinase does not require its known nuclear effectors. Upon selenite treatment, a null snf1 mutant displays higher levels of oxidized versus reduced glutathione compared to wild type cells, and its hypersensitivity to the agent is rescued by overexpression of the glutathione reductase gene GLR1. In the presence of agents such as diethyl maleate or diamide, which cause alterations in glutathione redox homeostasis by increasing the levels of oxidized glutathione, yeast cells also require Snf1 in an Elm1-dependent manner for growth. These observations demonstrate a role of Snf1 to protect yeast cells in situations where glutathione-dependent redox homeostasis is altered to a more oxidant intracellular environment and associates AMPK to responses against oxidative stress.
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