ArticleGenetics2002
The roles of REV3 and RAD57 in double-strand-break-repair-induced mutagenesis of Saccharomyces cerevisiae.
Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 103 citations in OpenAlex.
- Mutations and structural variants arising during double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Rad51 determines pathway usage in post-replication repair.Nature communications · 2026Article
- Meiotic DNA breaks drive multifaceted mutagenesis in the human germ line.Science (New York, N.Y.) · 2023Article
- Rad51 filaments assembled in the absence of the complex formed by the Rad51 paralogs Rad55 and Rad57 are outcompeted by translesion DNA polymerases on UV-induced ssDNA gaps.PLoS genetics · 2023Article
- Mechanism for inverted-repeat recombination induced by a replication fork barrier.Nature communications · 2022Article
- REV1 Inhibition Enhances Radioresistance and Autophagy.Cancers · 2021Article
- Review
- REV7: Jack of many trades.Trends in cell biology · 2021Review
- Non-recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance.EMBO reports · 2021Article
- A Rad51-independent pathway promotes single-strand template repair in gene editing.PLoS genetics · 2020Article
- Genetic Characterization of Three Distinct Mechanisms Supporting RNA-Driven DNA Repair and Modification Reveals Major Role of DNA Polymerase ζ.Molecular cell · 2020Article
- DNA polymerase ζ in DNA replication and repair.Nucleic acids research · 2019Review
- Translesion Synthesis in Plants: Ultraviolet Resistance and Beyond.Frontiers in plant science · 2019Review
- Repair of a Site-Specific DNA Cleavage: Old-School Lessons for Cas9-Mediated Gene Editing.ACS chemical biology · 2018Review
- Regulation of hetDNA Length during Mitotic Double-Strand Break Repair in Yeast.Molecular cell · 2017Article
- Eukaryotic DNA Polymerases in Homologous Recombination.Annual review of genetics · 2016Review
- Mutation at a distance caused by homopolymeric guanine repeats in Saccharomyces cerevisiae.Science advances · 2016Article
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- Elevated mutation rate during meiosis in Saccharomyces cerevisiae.PLoS genetics · 2015Article
- Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA synthesis associated with recombinational repair of chromosomal double-strand breaks (DSBs) has a lower fidelity than normal replicative DNA synthesis. Here, we use an inverted-repeat substrate to monitor the fidelity of repair of a site-specific DSB. DSB induction made by the HO endonuclease stimulates recombination >5000-fold and is associated with a >1000-fold increase in mutagenesis of an adjacent gene. We demonstrate that most break-repair-induced mutations (BRIMs) are point mutations and have a higher proportion of frameshifts than do spontaneous mutations of the same substrate. Although the REV3 translesion DNA polymerase is not required for recombination, it introduces approximately 75% of the BRIMs and approximately 90% of the base substitution mutations. Recombinational repair of the DSB is strongly dependent upon genes of the RAD52 epistasis group; however, the residual recombinants present in rad57 mutants are associated with a 5- to 20-fold increase in BRIMs. The spectrum of mutations in rad57 mutants is similar to that seen in the wild-type strain and is similarly affected by REV3. We also find that REV3 is required for the repair of MMS-induced lesions when recombinational repair is compromised. Our data suggest that Rad55p/Rad57p help limit the generation of substrates that require pol zeta during recombination.
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Registered trials
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.