ArticleNature communications2025
Rescuing the bacterial replisome at a nick requires recombinational repair and helicase reloading.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed.
- Single-molecule tracking of RNA-DNA hybrid removal enzymes important for lagging-strand replication.Biophysical journal · 2026Article
- Bacillus subtilis DnaB forms multiple protein-protein interactions essential for DNA replication initiation.Nucleic acids research · 2026Article
- 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
- Distinct repair outcomes from single and convergent replication fork collapse.Nature structural & molecular biology · 2026Article
- Processing of Reversed Replication Forks is Required for the Resolution of Replication-Transcription Conflicts.bioRxiv : the preprint server for biology · 2026Article
- Single-molecule tracking of RNA-DNA hybrid removal enzymes important for lagging-strand replication.bioRxiv : the preprint server for biology · 2025Article
- Rescuing the bacterial replisome at a nick requires recombinational repair and helicase reloading.Nature communications · 2025Article
- Conflicts between the DNA replication and repair machineries promote cell death in Gram-positive bacteria.Microbiology (Reading, England) · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
DNA damage occurs in all cells and must be repaired to maintain genome integrity. Many DNA lesions are targeted for removal by repair systems that excise the damage, thereby generating a temporary single-strand discontinuity in the chromosome. If DNA repair has not been completed prior to a round of genome duplication, the single-strand discontinuity (nick or gap) can be converted to a double-strand break (DSB) by an oncoming replication fork. Because the genomic location of nucleobase damage is stochastic, investigating the fate of replication machinery (replisome) at DNA repair sites with single-strand discontinuities has been limited. Here we address this issue by expressing Cas9 nickases in Bacillus subtilis to create site-specific single-strand discontinuities in a bacterial chromosome. We find that a nick in either leading or lagging strand arrests DNA replication, while the fate of the replicative helicase is distinct and depends upon the strand nicked. Genetic, biochemical, and single cell analyses indicate that replisome/nick encounters generate a single-end DSB which requires recombinational repair to enable PriA-dependent replication restart. Together this work defines the physiologically relevant pathway used by B. subtilis to reinitiate DNA synthesis following replication fork inactivation at a single-strand discontinuity.
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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 Socratic graph.