ArticleMolecular microbiology2011
Mismatch repair causes the dynamic release of an essential DNA polymerase from the replication fork.
Article in Molecular microbiology, 2011. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- The B. subtilis translesion polymerase Pol Y1 is not strongly recruited to sites of replication upon different types of DNA damage.PLoS genetics · 2026Article
- DnaE uses strand displacement synthesis during Okazaki fragment repair.bioRxiv : the preprint server for biology · 2026Article
- "ThebioRxiv : the preprint server for biology · 2026Article
- The mutational landscape of Bacillus subtilis conditional hypermutators shows how proofreading skews DNA polymerase error rates.Nucleic acids research · 2025Article
- Bacterial DNA excision repair pathways.Nature reviews. Microbiology · 2022Review
- Mismatch Repair: From Preserving Genome Stability to Enabling Mutation Studies in Real-Time Single Cells.Cells · 2021Review
- Visualizing bacterial DNA replication and repair with molecular resolution.Current opinion in microbiology · 2018Review
- Interactions of theOpen biology · 2017Article
- MutS2 Promotes Homologous Recombination in Bacillus subtilis.Journal of bacteriology · 2017Article
- Single-molecule motions and interactions in live cells reveal target search dynamics in mismatch repair.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The Eukaryotic Mismatch Recognition Complexes Track with the Replisome during DNA Synthesis.PLoS genetics · 2015Article
- Asymmetric Context-Dependent Mutation Patterns Revealed through Mutation-Accumulation Experiments.Molecular biology and evolution · 2015Article
- RecO and RecR are necessary for RecA loading in response to DNA damage and replication fork stress.Journal of bacteriology · 2014Article
- Antibiotics induce redox-related physiological alterations as part of their lethality.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- RecD2 helicase limits replication fork stress in Bacillus subtilis.Journal of bacteriology · 2014Article
- Functional interplay of DnaE polymerase, DnaG primase and DnaC helicase within a ternary complex, and primase to polymerase hand-off during lagging strand DNA replication in Bacillus subtilis.Nucleic acids research · 2013Article
- DnaN clamp zones provide a platform for spatiotemporal coupling of mismatch detection to DNA replication.Molecular microbiology · 2013Article
- DNA Mismatch Repair.EcoSal Plus · 2012Article
- Residues in the N-terminal domain of MutL required for mismatch repair in Bacillus subtilis.Journal of bacteriology · 2012Article
- DNA repair and genome maintenance in Bacillus subtilis.Microbiology and molecular biology reviews : MMBR · 2012Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mismatch repair (MMR) corrects DNA polymerase errors occurring during genome replication. MMR is critical for genome maintenance, and its loss increases mutation rates several hundred fold. Recent work has shown that the interaction between the mismatch recognition protein MutS and the replication processivity clamp is important for MMR in Bacillus subtilis. To further understand how MMR is coupled to DNA replication, we examined the subcellular localization of MMR and DNA replication proteins fused to green fluorescent protein (GFP) in live cells, following an increase in DNA replication errors. We demonstrate that foci of the essential DNA polymerase DnaE-GFP decrease following mismatch incorporation and that loss of DnaE-GFP foci requires MutS. Furthermore, we show that MutS and MutL bind DnaE in vitro, suggesting that DnaE is coupled to repair. We also found that DnaE-GFP foci decrease in vivo following a DNA damage-independent arrest of DNA synthesis showing that loss of DnaE-GFP foci is caused by perturbations to DNA replication. We propose that MutS directly contacts the DNA replication machinery, causing a dynamic change in the organization of DnaE at the replication fork during MMR. Our results establish a striking and intimate connection between MMR and the replicating DNA polymerase complex in vivo.
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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.