ArticleNucleic acids research2004
The post-replication repair RAD18 and RAD6 genes are involved in the prevention of spontaneous mutations caused by 7,8-dihydro-8-oxoguanine in Saccharomyces cerevisiae.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27 citing papers in PubMed, 53 citations in OpenAlex.
- New alternatives in photoprotection: Preparation and evaluation of lamellar silicate derivatives and their use as sunscreens.International journal of cosmetic science · 2026Article
- Unveiling the vital role of OGG1 in inflammation, vascular endothelial damage, and cell death in obstetric and gynecological diseases.Human cell · 2025Review
- 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024Review
- Detection of Primary DNA Lesions by Transient Changes in Mating Behavior in YeastInternational journal of molecular sciences · 2023Article
- OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022Review
- Genetic Control of Oxidative Mutagenesis inJournal of bacteriology · 2020Article
- Yeast-based assays for the functional characterization of cancer-associated variants of human DNA repair genes.Microbial cell (Graz, Austria) · 2020Review
- Biochemical reconstitution and genetic characterization of the major oxidative damage base excision DNA repair pathway in Thermococcus kodakarensis.DNA repair · 2020Article
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- Translesion DNA synthesis and mutagenesis in eukaryotes.Cold Spring Harbor perspectives in biology · 2013Review
- In vivo bypass of 8-oxodG.PLoS genetics · 2013Article
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- Role of AtPolζ, AtRev1 and AtPolη in γ ray-induced mutagenesis.Plant signaling & behavior · 2011Article
- The polymerase eta translesion synthesis DNA polymerase acts independently of the mismatch repair system to limit mutagenesis caused by 7,8-dihydro-8-oxoguanine in yeast.Molecular and cellular biology · 2009Article
- Mutation analysis of Rad18 in human cancer cell lines and non small cell lung cancer tissues.Journal of experimental & clinical cancer research : CR · 2009Article
- Role of PCNA-dependent stimulation of 3'-phosphodiesterase and 3'-5' exonuclease activities of human Ape2 in repair of oxidative DNA damage.Nucleic acids research · 2009Article
- The efficiency and fidelity of 8-oxo-guanine bypass by DNA polymerases delta and eta.Nucleic acids research · 2009Article
- PCNA monoubiquitylation and DNA polymerase eta ubiquitin-binding domain are required to prevent 8-oxoguanine-induced mutagenesis in Saccharomyces cerevisiae.Nucleic acids research · 2009Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
7,8-dihydro-8-oxoguanine (8-oxoG) is an abundant and mutagenic lesion produced in DNA exposed to free radicals and reactive oxygen species. In Saccharomyces cerevisiae, the OGG1 gene encodes the 8-oxoG DNA N-glycosylase/AP lyase (Ogg1), which is the functional homologue of the bacterial Fpg. Ogg1-deficient strains are spontaneous mutators that accumulate GC to TA transversions due to unrepaired 8-oxoG in DNA. In yeast, DNA mismatch repair (MMR) and translesion synthesis (TLS) by DNA polymerase eta also play a role in the prevention of the mutagenic effect of 8-oxoG. In the present study, we show the RAD18 and RAD6 genes that are required to initiate post-replication repair (PRR) are also involved in the prevention of mutations by 8-oxoG. Consistently, a synergistic increase in spontaneous CanR and Lys+ mutation rates is observed in the absence of Rad6 or Rad18 proteins in ogg1 mutant strains. Spectra of CaR mutations in ogg1 rad18 and ogg1 rad6 double mutants show a strong bias in the favor of GC to TA transversions, which are 137- and 189-fold higher than in the wild-type, respectively. The results also show that Poleta (RAD30 gene product) plays a critical role on the prevention of mutations at 8-oxoG, whereas Polzeta (REV3 gene product) does not. Our current model suggests that the Rad6-Rad18 complex targets Poleta at DNA gaps that result from the MMR-mediated excision of adenine mispaired with 8-oxoG, allowing error-free dCMP incorporation opposite to this lesion.
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