ArticleProceedings of the National Academy of Sciences of the United States of America2009
The mismatch repair system promotes DNA polymerase zeta-dependent translesion synthesis in yeast.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Divergent Roles of Canonical and Non-Canonical Mismatch Repair in Regulating Temozolomide Sensitivity in Glioblastoma.International journal of molecular sciences · 2026Review
- Signification and Application of Mutator and Antimutator Phenotype-Induced Genetic Variations in Evolutionary Adaptation and Cancer Therapeutics.Journal of microbiology (Seoul, Korea) · 2023Review
- Changes in the architecture and abundance of replication intermediates delineate the chronology of DNA damage tolerance pathways at UV-stalled replication forks in human cells.Nucleic acids research · 2022Article
- A Comprehensive View of Translesion Synthesis in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2020Review
- Article
- The absence of the catalytic domains of Saccharomyces cerevisiae DNA polymerase ϵ strongly reduces DNA replication fidelity.Nucleic acids research · 2019Article
- Genetic Control of Genomic Alterations Induced in Yeast by Interstitial Telomeric Sequences.Genetics · 2018Article
- Parallel analysis of ribonucleotide-dependent deletions produced by yeast Top1 in vitro and in vivo.Nucleic acids research · 2016Article
- The role of Drosophila mismatch repair in suppressing recombination between diverged sequences.Scientific reports · 2015Article
- Topoisomerase 1-dependent deletions initiated by incision at ribonucleotides are biased to the non-transcribed strand of a highly activated reporter.Nucleic acids research · 2015Article
- 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
- RNA∶DNA hybrids initiate quasi-palindrome-associated mutations in highly transcribed yeast DNA.PLoS genetics · 2013Article
- Distinct pathways for repairing mutagenic lesions induced by methylating and ethylating agents.Mutagenesis · 2013Article
- Review
- Article
- DNA polymerase ζ generates tandem mutations in immunoglobulin variable regions.The Journal of experimental medicine · 2012Article
- Formaldehyde-induced mutagenesis in Saccharomyces cerevisiae: molecular properties and the roles of repair and bypass systems.Mutation research · 2012Article
- Article
- Role for topoisomerase 1 in transcription-associated mutagenesis in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA lesions that block replication can be bypassed by error-prone or error-free mechanisms. Error-prone mechanisms rely on specialized translesion synthesis (TLS) DNA polymerases that directly replicate over the lesion, whereas error-free pathways use an undamaged duplex as a template for lesion bypass. In the yeast Saccharomyces cerevisiae, most mutagenic TLS of spontaneous and induced DNA damage relies on DNA polymerase zeta (Polzeta) activity. Here, we use a distinct mutational signature produced by Polzeta in a frameshift-reversion assay to examine the role of the yeast mismatch repair (MMR) system in regulating Polzeta-dependent mutagenesis. Whereas MMR normally reduces mutagenesis by removing errors introduced by replicative DNA polymerases, we find that the MMR system is required for Polzeta-dependent mutagenesis. In the absence of homologous recombination, however, the error-prone Polzeta pathway is not affected by MMR status. These results demonstrate that MMR promotes Polzeta-dependent mutagenesis by inhibiting an alternative, error-free pathway that depends on homologous recombination. Finally, in contrast to its ability to remove mistakes made by replicative DNA polymerases, we show that MMR fails to efficiently correct errors introduced by Polzeta.
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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.