ArticleThe Journal of cell biology2022
Differential metabolism of arsenicals regulates Fps1-mediated arsenite transport.
Article in The Journal of cell biology, 2022. 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, 8 citations in OpenAlex.
- Arsenic-sensing domain controls ACR3 transporter trafficking in Marchantia polymorpha.The Plant cell · 2026Article
- Arsenic binds to nuclear transport factors and disrupts nucleocytoplasmic transport.Journal of cell science · 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
- Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.Cellular and molecular life sciences : CMLS · 2023Review
- Etp1 confers arsenite resistance by affecting ACR3 expression.FEMS yeast research · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic is an environmental toxin that exists mainly as pentavalent arsenate and trivalent arsenite. Both forms activate the yeast SAPK Hog1 but with different consequences. We describe a mechanism by which cells distinguish between these arsenicals through one-step metabolism to differentially regulate the bidirectional glycerol channel Fps1, an adventitious port for arsenite. Cells exposed to arsenate reduce it to thiol-reactive arsenite, which modifies a set of cysteine residues in target proteins, whereas cells exposed to arsenite metabolize it to methylarsenite, which modifies an additional set of cysteine residues. Hog1 becomes arsenylated, which prevents it from closing Fps1. However, this block is overcome in cells exposed to arsenite through methylarsenylation of Acr3, an arsenite efflux pump that we found also regulates Fps1 directly. This adaptation allows cells to restrict arsenite entry through Fps1 and also allows its exit when produced from arsenate exposure. These results have broad implications for understanding how SAPKs activated by diverse stressors can drive stress-specific outputs.
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Registered trials
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