ArticleDNA repair2013
Exonuclease 1 preferentially repairs mismatches generated by DNA polymerase α.
Article in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- The nuclease activity of DNA2 promotes exonuclease 1-independent mismatch repair.The Journal of biological chemistry · 2022Article
- Frequency and patterns of ribonucleotide incorporation around autonomously replicating sequences in yeast reveal the division of labor of replicative DNA polymerases.Nucleic acids research · 2021Article
- Stringent Primer Termination by an Archaeo-Eukaryotic DNA Primase.Frontiers in microbiology · 2021Article
- Involvement of DNA mismatch repair in the maintenance of heterochromatic DNA stability in Saccharomyces cerevisiae.PLoS genetics · 2017Article
- Human DNA polymerase delta double-mutant D316A;E318A interferes with DNA mismatch repair in vitro.Nucleic acids research · 2017Article
- Alterations in cellular metabolism triggered byProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Interaction of proliferating cell nuclear antigen with PMS2 is required for MutLα activation and function in mismatch repair.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mechanisms in E. coli and Human Mismatch Repair (Nobel Lecture).Angewandte Chemie (International ed. in English) · 2016Review
- Article
- Eukaryotic genome instability in light of asymmetric DNA replication.Critical reviews in biochemistry and molecular biology · 2016Review
- Single-Molecule FRET to Measure Conformational Dynamics of DNA Mismatch Repair Proteins.Methods in enzymology · 2016Article
- New insights into the mechanism of DNA mismatch repair.Chromosoma · 2015Review
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- A novel POLE mutation associated with cancers of colon, pancreas, ovaries and small intestine.Familial cancer · 2015Article
- Exonuclease 1-dependent and independent mismatch repair.DNA repair · 2015Review
- Okazaki fragment maturation involves α-segment error editing by the mammalian FEN1/MutSα functional complex.The EMBO journal · 2015Article
- Quantifying the contributions of base selectivity, proofreading and mismatch repair to nuclear DNA replication in Saccharomyces cerevisiae.DNA repair · 2015Article
- Article
- FEN1-mediated α-segment error editing during Okazaki fragment maturation.Cell cycle (Georgetown, Tex.) · 2015Article
- Deposition of histone H2A.Z by the SWR-C remodeling enzyme prevents genome instability.DNA repair · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Saccharomyces cerevisiae EXO1 gene encodes a 5' exonuclease that participates in mismatch repair (MMR) of DNA replication errors. Deleting EXO1 was previously shown to increase mutation rates to a greater extent when combined with a mutator variant (pol3-L612M) of the lagging strand replicase, DNA polymerase δ (Pol δ), than when combined with a mutator variant (pol2-M644G) of the leading strand replicase, DNA polymerase ɛ (Pol ɛ). Here we confirm that result, and extend the approach to examine the effect of deleting EXO1 in a mutator variant (pol1-L868M) of Pol α, the proofreading-deficient and least accurate of the three nuclear replicases that is responsible for initiating Okazaki fragment synthesis. We find that deleting EXO1 increases the mutation rate in the Pol α mutator strain to a significantly greater extent than in the Pol δ or Pol ɛ mutator strains, thereby preferentially reducing the efficiency of MMR of replication errors generated by Pol α. Because these mismatches are closer to the 5' ends of Okazaki fragments than are mismatches made by Pol δ or Pol ɛ, the results not only support the previous suggestion that Exo1 preferentially excises lagging strand replication errors during mismatch repair, they further imply that the 5' ends serve as entry points for 5' excision of replication errors made by Pol α, and possibly as strand discrimination signals for MMR. Nonetheless, mutation rates in the Pol α mutator strain are 5- to 25-fold lower in an exo1Δ strain as compared to an msh2Δ strain completely lacking MMR, indicating that in the absence of Exo1, most replication errors made by Pol α can still be removed in an Msh2-dependent manner by other nucleases and/or by strand displacement.
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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.