ArticleScientific reports2016
The yeast Aft2 transcription factor determines selenite toxicity by controlling the low affinity phosphate transport system.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- TheInternational journal of molecular sciences · 2023Article
- Yeast Ppz1 protein phosphatase toxicity involves the alteration of multiple cellular targets.Scientific reports · 2020Article
- Selenium Biofortification of Crop Food by Beneficial Microorganisms.Journal of fungi (Basel, Switzerland) · 2020Review
- Phosphate Homeostasis - A Vital Metabolic Equilibrium Maintained Through the INPHORS Signaling Pathway.Frontiers in microbiology · 2020Review
- Improvement of selenium enrichment inBioengineered · 2019Article
- Nitrate and Phosphate Transporters Rescue Fluoride Toxicity in Yeast.Chemical research in toxicology · 2019Article
- Characterization of a Novel Porin-Like Protein, ExtI, from Geobacter sulfurreducens and Its Implication in the Reduction of Selenite and Tellurite.International journal of molecular sciences · 2018Article
- Comparative Transcriptomics Highlights New Features of the Iron Starvation Response in the Human PathogenFrontiers in microbiology · 2018Article
- Lack of 14-3-3 proteins in Saccharomyces cerevisiae results in cell-to-cell heterogeneity in the expression of Pho4-regulated genes SPL2 and PHO84.BMC genomics · 2017Article
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Authors and funding
6 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The yeast Saccharomyces cerevisiae is employed as a model to study the cellular mechanisms of toxicity and defense against selenite, the most frequent environmental selenium form. We show that yeast cells lacking Aft2, a transcription factor that together with Aft1 regulates iron homeostasis, are highly sensitive to selenite but, in contrast to aft1 mutants, this is not rescued by iron supplementation. The absence of Aft2 strongly potentiates the transcriptional responses to selenite, particularly for DNA damage- and oxidative stress-responsive genes, and results in intracellular hyperaccumulation of selenium. Overexpression of PHO4, the transcriptional activator of the PHO regulon under low phosphate conditions, partially reverses sensitivity and hyperaccumulation of selenite in a way that requires the presence of Spl2, a Pho4-controlled protein responsible for post-transcriptional downregulation of the low-affinity phosphate transporters Pho87 and Pho90. SPL2 expression is strongly downregulated in aft2 cells, especially upon selenite treatment. Selenite hypersensitivity of aft2 cells is fully rescued by deletion of PHO90, suggesting a major role for Pho90 in selenite uptake. We propose that the absence of Aft2 leads to enhanced Pho90 function, involving both Spl2-dependent and independent events and resulting in selenite hyperaccumulation and toxicity.
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