ArticleThe Journal of biological chemistry2014
Regression of replication forks stalled by leading-strand template damage: I. Both RecG and RuvAB catalyze regression, but RuvC cleaves the holliday junctions formed by RecG preferentially.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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
29 citing papers in PubMed.
- Termination of DNA replication drives genomic instability via multiple mechanisms.Nucleic acids research · 2026Article
- Transcription-replication collisions trigger high-fidelity replication reset.Nucleic acids research · 2025Article
- Hallmarks of DNA replication stress responses in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2025Review
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- The Biochemical Mechanism of Fork Regression in Prokaryotes and Eukaryotes-A Single Molecule Comparison.International journal of molecular sciences · 2022Review
- The rarA gene as part of an expanded RecFOR recombination pathway: Negative epistasis and synthetic lethality with ruvB, recG, and recQ.PLoS genetics · 2021Article
- Article
- Single-molecule insight into stalled replication fork rescue in Escherichia coli.Nucleic acids research · 2021Review
- DNA Helicase-SSB Interactions Critical to the Regression and Restart of Stalled DNA Replication forks inGenes · 2020Review
- Frequent template switching in postreplication gaps: suppression of deleterious consequences by the Escherichia coli Uup and RadD proteins.Nucleic acids research · 2020Article
- Bacillus subtilis RecA interacts with and loads RadA/Sms to unwind recombination intermediates during natural chromosomal transformation.Nucleic acids research · 2019Article
- Replication fork rescue in mammalian mitochondria.Scientific reports · 2019Article
- Movement of the RecG Motor Domain upon DNA Binding Is Required for Efficient Fork Reversal.International journal of molecular sciences · 2018Article
- Replication Fork Breakage and Restart in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2018Review
- The archaeal ATPase PINA interacts with the helicase Hjm via its carboxyl terminal KH domain remodeling and processing replication fork and Holliday junction.Nucleic acids research · 2018Article
- Lesion Bypass and the Reactivation of Stalled Replication Forks.Annual review of biochemistry · 2018Review
- RPA and RAD51: fork reversal, fork protection, and genome stability.Nature structural & molecular biology · 2018Review
- Main steps in DNA double-strand break repair: an introduction to homologous recombination and related processes.Chromosoma · 2018Review
- Template-switching during replication fork repair in bacteria.DNA repair · 2017Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The orderly progression of replication forks formed at the origin of replication in Escherichia coli is challenged by encounters with template damage, slow moving RNA polymerases, and frozen DNA-protein complexes that stall the fork. These stalled forks are foci for genomic instability and must be reactivated. Many models of replication fork reactivation invoke nascent strand regression as an intermediate in the processing of the stalled fork. We have investigated the replication fork regression activity of RecG and RuvAB, two proteins commonly thought to be involved in the process, using a reconstituted DNA replication system where the replisome is stalled by collision with leading-strand template damage. We find that both RecG and RuvAB can regress the stalled fork in the presence of the replisome and SSB; however, RuvAB generates a completely unwound product consisting of the paired nascent leading and lagging strands, whereas RuvC cleaves the Holliday junction generated by RecG-catalyzed fork regression. We also find that RecG stimulates RuvAB-catalyzed regression, presumably because it is more efficient at generating the initial Holliday junction from the stalled fork.
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Registered trials
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