ArticlePLoS genetics2012
Recovery of arrested replication forks by homologous recombination is error-prone.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 91 citations in OpenAlex.
- Transcription-replication conflict resolution by nuclear RNA interference.Molecular cell · 2025Article
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Review
- SUMO protease and proteasome recruitment at the nuclear periphery differently affect replication dynamics at arrested forks.Nucleic acids research · 2024Article
- Article
- Using Sister Chromatid Exchange Assay to Detect Homologous Recombination Deficiency in Epigenetically Deregulated Urothelial Carcinoma Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Creation and resolution of non-B-DNA structural impediments during replication.Critical reviews in biochemistry and molecular biology · 2022Article
- Stimulation of adaptive gene amplification by origin firing under replication fork constraint.Nucleic acids research · 2022Article
- A rapidly reversible mutation generates subclonal genetic diversity and unstable drug resistance.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Restarted replication forks are error-prone and cause CAG repeat expansions and contractions.PLoS genetics · 2021Article
- Live-cell single-molecule tracking highlights requirements for stable Smc5/6 chromatin association in vivo.eLife · 2021Article
- Review
- A Conserved Histone H3-H4 Interface Regulates DNA Damage Tolerance and Homologous Recombination during the Recovery from Replication Stress.Molecular and cellular biology · 2021Article
- Repression of a large number of genes requires interplay between homologous recombination and HIRA.Nucleic acids research · 2021Article
- Replication dynamics of recombination-dependent replication forks.Nature communications · 2021Article
- The nuclear pore primes recombination-dependent DNA synthesis at arrested forks by promoting SUMO removal.Nature communications · 2020Article
- Mechanisms of direct replication restart at stressed replisomes.DNA repair · 2020Review
- Disease-associated DNA2 nuclease-helicase protects cells from lethal chromosome under-replication.Nucleic acids research · 2020Article
- Homologous recombination and Mus81 promote replication completion in response to replication fork blockage.EMBO reports · 2020Article
- Genomic Instability in Fungal Plant Pathogens.Genes · 2020Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homologous recombination is a universal mechanism that allows repair of DNA and provides support for DNA replication. Homologous recombination is therefore a major pathway that suppresses non-homology-mediated genome instability. Here, we report that recovery of impeded replication forks by homologous recombination is error-prone. Using a fork-arrest-based assay in fission yeast, we demonstrate that a single collapsed fork can cause mutations and large-scale genomic changes, including deletions and translocations. Fork-arrest-induced gross chromosomal rearrangements are mediated by inappropriate ectopic recombination events at the site of collapsed forks. Inverted repeats near the site of fork collapse stimulate large-scale genomic changes up to 1,500 times over spontaneous events. We also show that the high accuracy of DNA replication during S-phase is impaired by impediments to fork progression, since fork-arrest-induced mutation is due to erroneous DNA synthesis during recovery of replication forks. The mutations caused are small insertions/duplications between short tandem repeats (micro-homology) indicative of replication slippage. Our data establish that collapsed forks, but not stalled forks, recovered by homologous recombination are prone to replication slippage. The inaccuracy of DNA synthesis does not rely on PCNA ubiquitination or trans-lesion-synthesis DNA polymerases, and it is not counteracted by mismatch repair. We propose that deletions/insertions, mediated by micro-homology, leading to copy number variations during replication stress may arise by progression of error-prone replication forks restarted by homologous recombination.
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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.