ArticleProceedings of the National Academy of Sciences of the United States of America1998
The role of mismatch repair in the prevention of base pair mutations in Saccharomyces cerevisiae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed, 88 citations in OpenAlex.
- A mitochondria-specific mutational signature of aging: increased rate of A > G substitutions on the heavy strand.Nucleic acids research · 2022Article
- Development of an MSI-positive colon tumor with aberrant DNA methylation in a PPAP patient.Journal of human genetics · 2019Article
- DNA mismatch repair preferentially protects genes from mutation.Genome research · 2018Article
- The Major Replicative Histone Chaperone CAF-1 Suppresses the Activity of the DNA Mismatch Repair System in the Cytotoxic Response to a DNA-methylating Agent.The Journal of biological chemistry · 2016Article
- Understanding how mismatch repair proteins participate in the repair/anti-recombination decision.FEMS yeast research · 2016Article
- DNA Mismatch Repair Interacts with CAF-1- and ASF1A-H3-H4-dependent Histone (H3-H4)2 Tetramer Deposition.The Journal of biological chemistry · 2016Article
- Review
- Non-canonical actions of mismatch repair.DNA repair · 2016Review
- Replicative DNA polymerase δ but not ε proofreads errors in Cis and in Trans.PLoS genetics · 2015Article
- Eukaryotic Mismatch Repair in Relation to DNA Replication.Annual review of genetics · 2015Review
- Oxidative stress and its significant roles in neurodegenerative diseases and cancer.International journal of molecular sciences · 2014Review
- Kinetics, structure, and mechanism of 8-Oxo-7,8-dihydro-2'-deoxyguanosine bypass by human DNA polymerase η.The Journal of biological chemistry · 2014Article
- Article
- In vivo bypass of 8-oxodG.PLoS genetics · 2013Article
- The JmjC domain histone demethylase Ndy1 regulates redox homeostasis and protects cells from oxidative stress.Molecular and cellular biology · 2008Article
- Sequence divergence impedes crossover more than noncrossover events during mitotic gap repair in yeast.Genetics · 2008Article
- Oxygen metabolism and reactive oxygen species cause chromosomal rearrangements and cell death.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Specialized mismatch repair function of Glu339 in the Phe-X-Glu motif of yeast Msh6.DNA repair · 2007Article
- Physical and functional interactions between Escherichia coli MutY glycosylase and mismatch repair protein MutS.Journal of bacteriology · 2007Article
- Transcriptome analysis of Aspergillus nidulans exposed to camptothecin-induced DNA damage.Eukaryotic cell · 2006Article
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
In most organisms, the mismatch repair (MMR) system plays an important role in substantially lowering mutation rates and blocking recombination between nonidentical sequences. In Saccharomyces cerevisiae, the products of three genes homologous to Escherichia coli mutS-MSH2, MSH3, and MSH6-function in MMR by recognizing mispaired bases. To determine the effect of MMR on single-base pair mismatches, we have measured reversion rates of specific point mutations in the CYC1 gene in both wild-type and MMR-deficient strains. The reversion rates of all of the point mutations are similar in wild-type cells. However, we find that in the absence of MSH2 or MSH6, but not MSH3, reversion rates of some mutations are increased by up to 60,000-fold, whereas reversion rates of other mutations are essentially unchanged. When cells are grown anaerobically, the reversion rates in MMR-deficient strains are decreased by as much as a factor of 60. We suggest that the high reversion rates observed in these MMR-deficient strains are caused by misincorporations opposite oxidatively damaged bases and that MMR normally prevents these mutations. We further suggest that recognition of mispairs opposite damaged bases may be a more important role for MMR in yeast than correction of errors opposite normal bases.
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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.