ArticleNature2013
Avoiding chromosome pathology when replication forks collide.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 134 citations in OpenAlex.
- Processing of reversed replication forks is required for the resolution of replication-transcription conflicts.Nucleic acids research · 2026Article
- Topoisomerase III limits RecA-dependent DNA amplification in the chromosome terminus with RecG.Nucleic acids research · 2026Article
- The bacterial MRE11-RAD50 and DNA2-WRN homologs process replication forks at distinct and separate loci on the chromosome.FEBS letters · 2026Article
- Termination of DNA replication drives genomic instability via multiple mechanisms.Nucleic acids research · 2026Article
- Mechanisms of chromosomal DNA replication in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2026Review
- Conflicts between the DNA replication and repair machineries promote cell death in Gram-positive bacteria.Microbiology (Reading, England) · 2025Article
- Topo IV is required to allow replisomes to converge and complete replication on the chromosome.PLoS genetics · 2025Article
- Inducible genome-wide mutagenesis for improvement of pDNA production by E. coli.Microbial cell factories · 2025Article
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- Escherichia coli DNA replication: the old model organism still holds many surprises.FEMS microbiology reviews · 2024Review
- Review
- Gene duplication and deletion caused by over-replication at a fork barrier.Nature communications · 2023Article
- RecA and SSB genome-wide distribution in ssDNA gaps and ends in Escherichia coli.Nucleic acids research · 2023Article
- Replication fork binding triggers structural changes in the PriA helicase that govern DNA replication restart in E. coli.Nature communications · 2023Article
- Characterization of a pathway of genomic instability induced by R-loops and its regulation by topoisomerases in E. coli.PLoS genetics · 2023Article
- The in vivo measurement of replication fork velocity and pausing by lag-time analysis.Nature communications · 2023Article
- Interplay between chromosomal architecture and termination of DNA replication in bacteria.Frontiers in microbiology · 2023Review
- Robust linear DNA degradation supports replication-initiation-defective mutants in Escherichia coli.G3 (Bethesda, Md.) · 2022Article
- Role for DNA double strand end-resection activity of RecBCD in control of aberrant chromosomal replication initiation in Escherichia coli.Nucleic acids research · 2022Article
- Speed variations of bacterial replisomes.eLife · 2022Article
30 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
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Chromosome duplication normally initiates through the assembly of replication fork complexes at defined origins. DNA synthesis by any one fork is thought to cease when it meets another travelling in the opposite direction, at which stage the replication machinery may simply dissociate before the nascent strands are finally ligated. But what actually happens is not clear. Here we present evidence consistent with the idea that every fork collision has the potential to threaten genomic integrity. In Escherichia coli this threat is kept at bay by RecG DNA translocase and by single-strand DNA exonucleases. Without RecG, replication initiates where forks meet through a replisome assembly mechanism normally associated with fork repair, replication restart and recombination, establishing new forks with the potential to sustain cell growth and division without an active origin. This potential is realized when roadblocks to fork progression are reduced or eliminated. It relies on the chromosome being circular, reinforcing the idea that replication initiation is triggered repeatedly by fork collision. The results reported raise the question of whether replication fork collisions have pathogenic potential for organisms that exploit several origins to replicate each chromosome.
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What OpenQuestion holds
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.