ArticlePLoS genetics2009
Peroxiredoxin Tsa1 is the key peroxidase suppressing genome instability and protecting against cell death in Saccharomyces cerevisiae.
Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 68 citations in OpenAlex.
- Time-resolved monitoring of yeast responses to lipopolysaccharide exposure by cell-released volatile organic compounds.Applied and environmental microbiology · 2025Article
- Deficits in mitochondrial dynamics and iron balance result in templated insertions.Nature communications · 2025Article
- RNA-DNA Differences: Mechanisms, Oxidative Stress, Transcriptional Fidelity, and Health Implications.Antioxidants (Basel, Switzerland) · 2025Review
- AoPrdx2 Regulates Oxidative Stress, Reactive Oxygen Species, Trap Formation, and Secondary Metabolism inJournal of fungi (Basel, Switzerland) · 2024Article
- Peroxiredoxins couple metabolism and cell division in an ultradian cycle.Nature chemical biology · 2021Article
- Trajectory and uniqueness of mutational signatures in yeast mutators.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Wine yeast peroxiredoxinMicroorganisms · 2020Article
- Genomic Instability and Cellular Senescence: Lessons From the Budding Yeast.Frontiers in cell and developmental biology · 2020Review
- Hyperoxidation of mitochondrial peroxiredoxin limits HThe EMBO journal · 2019Article
- Piecing Together How Peroxiredoxins Maintain Genomic Stability.Antioxidants (Basel, Switzerland) · 2018Review
- Expression of oxidized protein tyrosine phosphatase and γH2AX predicts poor survival of gastric carcinoma patients.BMC cancer · 2018Article
- Thioredoxin and Glutaredoxin Systems Required for Oxidative Stress Resistance, Fungicide Sensitivity, and Virulence of Alternaria alternata.Applied and environmental microbiology · 2018Article
- AID and Reactive Oxygen Species Can Induce DNA Breaks within Human Chromosomal Translocation Fragile Zones.Molecular cell · 2017Article
- Enhanced fermentative performance under stresses of multiple lignocellulose-derived inhibitors by overexpression of a typical 2-Cys peroxiredoxin fromBiotechnology for biofuels · 2017Article
- Mitochondrial proteomics of the acetic acid - induced programmed cell death response in a highly tolerantMicrobial cell (Graz, Austria) · 2016Article
- Adaptive aneuploidy protects against thiol peroxidase deficiency by increasing respiration via key mitochondrial proteins.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- A peroxiredoxin, PRDX-2, is required for insulin secretion and insulin/IIS-dependent regulation of stress resistance and longevity.Aging cell · 2015Article
- Oxidative stress in fungi: its function in signal transduction, interaction with plant hosts, and lignocellulose degradation.Biomolecules · 2015Review
- Oxidative stress conditions increase the frequency of de novo formation of the yeast [PSI+] prion.Molecular microbiology · 2015Article
- Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Peroxiredoxins (Prxs) constitute a family of thiol-specific peroxidases that utilize cysteine (Cys) as the primary site of oxidation during the reduction of peroxides. To gain more insight into the physiological role of the five Prxs in budding yeast Saccharomyces cerevisiae, we performed a comparative study and found that Tsa1 was distinguished from the other Prxs in that by itself it played a key role in maintaining genome stability and in sustaining aerobic viability of rad51 mutants that are deficient in recombinational repair. Tsa2 and Dot5 played minor but distinct roles in suppressing the accumulation of mutations in cooperation with Tsa1. Tsa2 was capable of largely complementing the absence of Tsa1 when expressed under the control of the Tsa1 promoter. The presence of peroxidatic cysteine (Cys(47)) was essential for Tsa1 activity, while Tsa1(C170S) lacking the resolving Cys was partially functional. In the absence of Tsa1 activity (tsa1 or tsa1(CCS) lacking the peroxidatic and resolving Cys) and recombinational repair (rad51), dying cells displayed irregular cell size/shape, abnormal cell cycle progression, and significant increase of phosphatidylserine externalization, an early marker of apoptosis-like cell death. The tsa1(CCS) rad51- or tsa1 rad51-induced cell death did not depend on the caspase Yca1 and Ste20 kinase, while the absence of the checkpoint protein Rad9 accelerated the cell death processes. These results indicate that the peroxiredoxin Tsa1, in cooperation with appropriate DNA repair and checkpoint mechanisms, acts to protect S. cerevisiae cells against toxic levels of DNA damage that occur during aerobic growth.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.