ArticleScientific reports2015
Loss of APD1 in yeast confers hydroxyurea sensitivity suppressed by Yap1p transcription factor.
Article in Scientific reports, 2015. 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, 11 citations in OpenAlex.
- Requirements for the biogenesis of [2Fe-2S] proteins in the human and yeast cytosol.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Molecular Response ofJournal of fungi (Basel, Switzerland) · 2023Article
- Genetically induced redox stress occurs in a yeast model for Roberts syndrome.G3 (Bethesda, Md.) · 2022Article
- Heme deficiency sensitizes yeast cells to oxidative stress induced by hydroxyurea.The Journal of biological chemistry · 2017Article
- The Cell Killing Mechanisms of Hydroxyurea.Genes · 2016Review
- SIRT1 Suppresses Human T-Cell Leukemia Virus Type 1 Transcription.Journal of virology · 2015Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Ferredoxins are iron-sulfur proteins that play important roles in electron transport and redox homeostasis. Yeast Apd1p is a novel member of the family of thioredoxin-like ferredoxins. In this study, we characterized the hydroxyurea (HU)-hypersensitive phenotype of apd1Δ cells. HU is an inhibitor of DNA synthesis, a cellular stressor and an anticancer agent. Although the loss of APD1 did not influence cell proliferation or cell cycle progression, it resulted in HU sensitivity. This sensitivity was reverted in the presence of antioxidant N-acetyl-cysteine, implicating a role for intracellular redox. Mutation of the iron-binding motifs in Apd1p abrogated its ability to rescue HU sensitivity in apd1Δ cells. The iron-binding activity of Apd1p was verified by a color assay. By mass spectrometry two irons were found to be incorporated into one Apd1p protein molecule. Surprisingly, ribonucleotide reductase genes were not induced in apd1Δ cells and the HU sensitivity was unaffected when dNTP production was boosted. A suppressor screen was performed and the expression of stress-regulated transcription factor Yap1p was found to effectively rescue the HU sensitivity in apd1Δ cells. Taken together, our work identified Apd1p as a new ferredoxin which serves critical roles in cellular defense against HU.
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