ArticlePLoS genetics2012
Replication fork reversal after replication-transcription collision.
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 80 papers.
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Who cites it
80 citing papers in PubMed, 114 citations in OpenAlex.
- Processing of reversed replication forks is required for the resolution of replication-transcription conflicts.Nucleic acids research · 2026Article
- Processing of Reversed Replication Forks is Required for the Resolution of Replication-Transcription Conflicts.bioRxiv : the preprint server for biology · 2026Article
- Transcription-replication collisions trigger high-fidelity replication reset.Nucleic acids research · 2025Article
- The bacterial transcription terminator, Rho, functions as an RNA:DNA hybrid (RDH) helicase in vivo.The Biochemical journal · 2025Article
- UV induces codirectional replication-transcription conflicts and an alternative DnaA-dependent replication origin in the rnhAB mutants of Escherichiacoli.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
- The effect of site-specific recombinases XerCD on the removal of over-replicated chromosomal DNA through outer membrane vesicles in bacteria.Microbiology spectrum · 2024Article
- Processing of stalled replication forks in Bacillus subtilis.FEMS microbiology reviews · 2024Review
- The chromatin network helps prevent cancer-associated mutagenesis at transcription-replication conflicts.Nature communications · 2023Article
- RNase H genes cause distinct impacts on RNA:DNA hybrid formation and mutagenesis genome wide.Science advances · 2023Article
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- RNase H genes cause distinct impacts on RNA:DNA hybrid formation and mutagenesis genome-wide.bioRxiv : the preprint server for biology · 2023Article
- Article
- Interplay between chromosomal architecture and termination of DNA replication in bacteria.Frontiers in microbiology · 2023Review
- Beneficial and detrimental genes in the cellular response to replication arrest.PLoS genetics · 2022Article
- The Impact of RNA-DNA Hybrids on Genome Integrity in Bacteria.Annual review of microbiology · 2022Review
- Role for DNA double strand end-resection activity of RecBCD in control of aberrant chromosomal replication initiation in Escherichia coli.Nucleic acids research · 2022Article
- Escherichia coli cell factories with altered chromosomal replication scenarios exhibit accelerated growth and rapid biomass production.Microbial cell factories · 2022Article
- RadD is a RecA-dependent accessory protein that accelerates DNA strand exchange.Nucleic acids research · 2022Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Replication fork arrest is a recognized source of genetic instability, and transcription is one of the most prominent causes of replication impediment. We analyze here the requirement for recombination proteins in Escherichia coli when replication-transcription head-on collisions are induced at a specific site by the inversion of a highly expressed ribosomal operon (rrn). RecBC is the only recombination protein required for cell viability under these conditions of increased replication-transcription collisions. In its absence, fork breakage occurs at the site of collision, and the resulting linear DNA is not repaired and is slowly degraded by the RecJ exonuclease. Lethal fork breakage is also observed in cells that lack RecA and RecD, i.e. when both homologous recombination and the potent exonuclease V activity of the RecBCD complex are inactivated, with a slow degradation of the resulting linear DNA by the combined action of the RecBC helicase and the RecJ exonuclease. The sizes of the major linear fragments indicate that DNA degradation is slowed down by the encounter with another rrn operon. The amount of linear DNA decreases nearly two-fold when the Holliday junction resolvase RuvABC is inactivated in recB, as well as in recA recD mutants, indicating that part of the linear DNA is formed by resolution of a Holliday junction. Our results suggest that replication fork reversal occurs after replication-transcription head-on collision, and we propose that it promotes the action of the accessory replicative helicases that dislodge the obstacle.
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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.