ArticleNucleic acids research2025
Transcription-replication collisions trigger high-fidelity replication reset.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Processing of reversed replication forks is required for the resolution of replication-transcription conflicts.Nucleic acids research · 2026Article
- Distinct repair outcomes from single and convergent replication fork collapse.Nature structural & molecular biology · 2026Article
- The ω subunit stabilizes transcribing RNA polymerase to balance processivity and collision resolution.bioRxiv : the preprint server for biology · 2026Article
- Processing of Reversed Replication Forks is Required for the Resolution of Replication-Transcription Conflicts.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Double-stranded DNA ends arise from external agents or cellular processes like transcription-replication collisions (TRCs), threatening genome stability. Here, we performed genomic CRISPRi screens to uncover DNA end formation factors in Escherichia coli. We discovered that translation-transcription decoupling causes DNA end formation through a TRC-dependent pathway, which is lethal when DNA end processing by RecBCD is disrupted, but not when recombination is disrupted. We find that TRCs cause replisome stalling followed by "rear-ending" from trailing replisomes which generates free DNA ends, rather than strand breaks. Surprisingly, these DNA ends are resolved through a process we call "replication reset", where the stalled replicore is degraded, without triggering recombination, the DNA damage response, or mutagenesis. This hidden replicore-degradation resets the replication cycle without consequence for the genome. This discovery reveals a novel DNA safeguard mechanism for preserving genome stability when replication is disturbed and challenges the notion that TRCs necessarily cause genome instability in bacteria.
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Registered trials
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