ArticleGenetics1997
A role for REV3 in mutagenesis during double-strand break repair in Saccharomyces cerevisiae.
Article in Genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 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
100 citing papers in PubMed, 200 citations in OpenAlex.
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Pif1 family helicases promote mutation avoidance during DNA replication.Nucleic acids research · 2022Article
- Host translesion polymerases are required for viral genome integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Single-strand template repair: key insights to increase the efficiency of gene editing.Current genetics · 2021Review
- REV7: Jack of many trades.Trends in cell biology · 2021Review
- A Rad51-independent pathway promotes single-strand template repair in gene editing.PLoS genetics · 2020Article
- Timing of appearance of new mutations during yeast meiosis and their association with recombination.Current genetics · 2020Article
- DNA polymerase ζ in DNA replication and repair.Nucleic acids research · 2019Review
- Mutations in the S-Adenosylmethionine Synthetase GenesGenetics · 2019Article
- Identification of potentially novel functions of DNA polymerase zeta catalytic subunit in oriental river prawn,3 Biotech · 2019Article
- What is mutation? A chapter in the series: How microbes "jeopardize" the modern synthesis.PLoS genetics · 2019Review
- Translesion Synthesis in Plants: Ultraviolet Resistance and Beyond.Frontiers in plant science · 2019Review
- Identifying Drivers of Parallel Evolution: A Regression Model Approach.Genome biology and evolution · 2018Article
- Repair of a Site-Specific DNA Cleavage: Old-School Lessons for Cas9-Mediated Gene Editing.ACS chemical biology · 2018Review
- Article
- Translesion DNA Synthesis in Cancer: Molecular Mechanisms and Therapeutic Opportunities.Chemical research in toxicology · 2017Review
- Stress-Induced Mutagenesis: Implications in Cancer and Drug Resistance.Annual review of cancer biology · 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
- Error-Prone Repair of DNA Double-Strand Breaks.Journal of cellular physiology · 2016Review
40 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recombinational repair of double-strand breaks (DSBs), traditionally believed to be an error-free DNA repair pathway, was recently shown to increase the frequency of mutations in a nearby interval. The reversion rate of trp1 alleles (either nonsense or frameshift mutations) near an HO-endonuclease cleavage site is increased at least 100-fold among cells that have experienced an HO-mediated DSB. We report here that in strains deleted for rev3 this DSB-associated reversion of a nonsense mutation was greatly decreased. Thus REV3, which encodes a subunit of the translesion DNA polymerase zeta, was responsible for the majority of these base substitution errors near a DSB. However, rev3 strains showed no decrease in HO-stimulated recombination, implying that another DNA polymerase also functioned in recombinational repair of a DSB. Reversion of trp1 frameshift alleles near a DSB was not reduced in rev3 strains, indicating that another polymerase could act during DSB repair to make these frameshift errors. Analysis of spontaneous reversion in haploid strains suggested that Rev3p had a greater role in making point mutations than in frameshift mutations.
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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.