ArticleMolecular biology of the cell2019
Methylated metabolite of arsenite blocks glycerol production in yeast by inhibition of glycerol-3-phosphate dehydrogenase.
Article in Molecular biology of the cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Decoding the metabolic cipher of dormant cancer cells: molecular mechanisms and therapeutic potentials.Cell communication and signaling : CCS · 2026Review
- Arsenic binds to nuclear transport factors and disrupts nucleocytoplasmic transport.Journal of cell science · 2025Article
- Hog1 plays a role in regulating lipid droplet homeostasis.Archives of microbiology · 2025Article
- Direct binding of arsenicals to nuclear transport factors disrupts nucleocytoplasmic transport.bioRxiv : the preprint server for biology · 2025Article
- Acetic acid-induced stress granules function as scaffolding complexes for Hog1 activation by Pbs2.The Journal of cell biology · 2025Article
- Identification of potential modulators for human GPD1 by docking-based virtual screening, molecular dynamics simulations, binding free energy calculations, and DeLA-drug analysis.Scientific reports · 2024Article
- Etp1 confers arsenite resistance by affecting ACR3 expression.FEMS yeast research · 2022Article
- Differential metabolism of arsenicals regulates Fps1-mediated arsenite transport.The Journal of cell biology · 2022Article
- Rapid and reversible cell volume changes in response to osmotic stress in yeast.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021Article
- The Third International Symposium on Fungal Stress - ISFUS.Fungal biology · 2020Article
- Crosstalk between Saccharomycescerevisiae SAPKs Hog1 and Mpk1 is mediated by glycerol accumulation.Fungal biology · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The yeast high-osmolarity glycerol (HOG) stress-activated protein kinase Hog1 is activated in response to hyperosmotic stress, inducing the production and retention of glycerol to restore osmotic balance. Hog1 promotes retention of glycerol through closure of the plasma-membrane glycerol channel Fps1. Treatment of yeast with the toxic trivalent metalloid arsenite (As(III)) also activates Hog1 as part of a protective response in which Hog1 closes Fps1, the main entry port for As(III). In this study, we investigated how cells treated with As(III) avoid creating a new stress caused by the accumulation of glycerol in the absence of hyperosmotic stress conditions. We found that As(III) treatment did not induce glycerol accumulation and, in fact, blocked the accumulation of glycerol induced by constitutive Hog1 activity. We demonstrated that As(III) blocks glycerol production indirectly after its metabolic activation to methylarsenite (MAs(III)), which is a potent inhibitor of glycerol-3-phosphate dehydrogenase. Finally, we used a biotinylated arsenic probe to establish that Cys306 of yeast Gpd1, a highly conserved residue within the active site, is the key target of MAs(III). Conservative mutations at this residue greatly diminished Gpd1 activity. This study offers insight into mechanisms by which SAPK outputs are tailored to specific stressors.
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