ArticleGenetics2013
The mechanism of nucleotide excision repair-mediated UV-induced mutagenesis in nonproliferating cells.
Article in Genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Detection of "hidden" mitotic crossovers by long-read DNA sequencing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Mutations and mitotic recombination events in nondividing cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mitotic recombination events and single-base mutations induced by ultraviolet light in G1-arrested yeast cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genome-wide maps of UV damage repair and mutation suppression by CPD photolyase.Nucleic acids research · 2025Article
- Article
- Oxidative stress drives mutagenesis through transcription-coupled repair in bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Genetic control of the error-prone repair of a chromosomal double-strand break with 5' overhangs in yeast.bioRxiv : the preprint server for biology · 2023Article
- Article
- Replication-independent instability of Friedreich's ataxia GAA repeats during chronological aging.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- Regulation of UV damage repair in quiescent yeast cells.DNA repair · 2020Article
- Processing closely spaced lesions during Nucleotide Excision Repair triggers mutagenesis in E. coli.PLoS genetics · 2017Article
- Recombination Is Responsible for the Increased Recovery of Drug-Resistant Mutants with Hypermutated Genomes in Resting Yeast Diploids Expressing APOBEC Deaminases.Frontiers in genetics · 2017Article
- Insulin-like growth factor-1 receptor regulates repair of ultraviolet B-induced DNA damage in human keratinocytes in vivo.Molecular oncology · 2016Article
- Coordination of DNA damage tolerance mechanisms with cell cycle progression in fission yeast.Cell cycle (Georgetown, Tex.) · 2016Article
- Eukaryotic DNA polymerase ζ.DNA repair · 2015Review
- DNA polymerase ζ-dependent lesion bypass in Saccharomyces cerevisiae is accompanied by error-prone copying of long stretches of adjacent DNA.PLoS genetics · 2015Article
- Shared genetic pathways contribute to the tolerance of endogenous and low-dose exogenous DNA damage in yeast.Genetics · 2014Article
- Replicating damaged DNA in eukaryotes.Cold Spring Harbor perspectives in biology · 2013Review
- Illuminating genome repair by photolyase.Photochemistry and photobiologyArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Following the irradiation of nondividing yeast cells with ultraviolet (UV) light, most induced mutations are inherited by both daughter cells, indicating that complementary changes are introduced into both strands of duplex DNA prior to replication. Early analyses demonstrated that such two-strand mutations depend on functional nucleotide excision repair (NER), but the molecular mechanism of this unique type of mutagenesis has not been further explored. In the experiments reported here, an ade2 adeX colony-color system was used to examine the genetic control of UV-induced mutagenesis in nondividing cultures of Saccharomyces cerevisiae. We confirmed a strong suppression of two-strand mutagenesis in NER-deficient backgrounds and demonstrated that neither mismatch repair nor interstrand crosslink repair affects the production of these mutations. By contrast, proteins involved in the error-prone bypass of DNA damage (Rev3, Rev1, PCNA, Rad18, Pol32, and Rad5) and in the early steps of the DNA-damage checkpoint response (Rad17, Mec3, Ddc1, Mec1, and Rad9) were required for the production of two-strand mutations. There was no involvement, however, for the Pol η translesion synthesis DNA polymerase, the Mms2-Ubc13 postreplication repair complex, downstream DNA-damage checkpoint factors (Rad53, Chk1, and Dun1), or the Exo1 exonuclease. Our data support models in which UV-induced mutagenesis in nondividing cells occurs during the Pol ζ-dependent filling of lesion-containing, NER-generated gaps. The requirement for specific DNA-damage checkpoint proteins suggests roles in recruiting and/or activating factors required to fill such gaps.
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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.