ArticleProceedings of the National Academy of Sciences of the United States of America2007
Oxygen metabolism and reactive oxygen species cause chromosomal rearrangements and cell death.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 100 citations in OpenAlex.
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- Trajectory and uniqueness of mutational signatures in yeast mutators.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- DNA damage induces Yap5-dependent transcription of ECO1/CTF7 in Saccharomyces cerevisiae.PloS one · 2020Article
- Co-Operation between Aneuploidy and Metabolic Changes in Driving Tumorigenesis.International journal of molecular sciences · 2019Review
- DNA damage response activates respiration and thereby enlarges dNTP pools to promote cell survival in budding yeast.The Journal of biological chemistry · 2019Article
- Cooperation between non-essential DNA polymerases contributes to genome stability in Saccharomyces cerevisiae.DNA repair · 2019Article
- Synthetic lethal interaction between oxidative stress response and DNA damage repair in the budding yeast and its application to targeted anticancer therapy.Journal of microbiology (Seoul, Korea) · 2019Review
- Peroxiredoxin Involvement in the Initiation and Progression of Human Cancer.Antioxidants & redox signaling · 2018Review
- Genome-wide map of Apn1 binding sites under oxidative stress in Saccharomyces cerevisiae.Yeast (Chichester, England) · 2017Article
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The absence of Tsa1, a key peroxiredoxin that functions to scavenge H(2)O(2) in Saccharomyces cerevisiae, causes the accumulation of a broad spectrum of mutations including gross chromosomal rearrangements (GCRs). Deletion of TSA1 also causes synthetic lethality in combination with mutations in RAD6 and several key genes involved in DNA double-strand break repair. In the present study we investigated the causes of GCRs and cell death in these mutants. tsa1-associated GCRs were independent of the activity of the translesion DNA polymerases zeta, eta, and Rev1. Anaerobic growth reduced substantially GCR rates of WT and tsa1 mutants and restored the viability of tsa1 rad6, tsa1 rad51, and tsa1 mre11 double mutants. Anaerobic growth also reduced the GCR rate of rad27, pif1, and rad52 mutants, indicating a role of reactive oxygen species in GCR formation in these mutants. In addition, deletion of TSA1 or H(2)O(2) treatment of WT cells resulted in increased formation of Rad52 foci, sites of repair of multiple DNA lesions. H(2)O(2) treatment also induced the GCRs. Our results provide in vivo evidence that oxygen metabolism and reactive oxygen species are important sources of DNA damages that can lead to GCRs and lethal effects in S. cerevisiae.
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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.