ArticleCell2017
Replication-Transcription Conflicts Generate R-Loops that Orchestrate Bacterial Stress Survival and Pathogenesis.
Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.
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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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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
177 citing papers in PubMed, 1 synthesis or guideline pooled it, 259 citations in OpenAlex.
- Synthetic lethal mutants inJournal of bacteriology · 2023Pooled it
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- Geometry of braided DNA dictates supercoiling partitioning.Nature communications · 2026Article
- Type III CRISPR-Cas systems preferentially acquire spacers from early-expressed phage genes in a transcription-dependent manner.Nucleic acids research · 2026Article
- Single-molecule tracking of RNA-DNA hybrid removal enzymes important for lagging-strand replication.Biophysical journal · 2026Article
- A self-replicating artificial module-genome that generates bacterial chromosome replication system in vitro.Nucleic acids research · 2026Article
- Processing of reversed replication forks is required for the resolution of replication-transcription conflicts.Nucleic acids research · 2026Article
- Polynucleotide Phosphorylase Stops Replication Restart by Degrading the RNA within R-loops during Replication-Transcription Conflicts.bioRxiv : the preprint server for biology · 2026Article
- Polymerase face-off: emerging concepts in transcription-replication coordination.EMBO reports · 2026Review
- Distinct mechanisms of replication stress induced by oncogenic RAS and cyclin E1 converge on R-loop-dependent fork reversal.Nature communications · 2026Article
- Processing of Reversed Replication Forks is Required for the Resolution of Replication-Transcription Conflicts.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial remodeling and metabolic reprogramming drive long-term salinity adaptation inmSystems · 2026Article
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- The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts.Nucleic acids research · 2026Article
- Real-time imaging of rotation during synthesis by the replisome.Science advances · 2026Article
- Alternative nucleic acid structures in microbial biology: regulatory functions and antimicrobial opportunities.Frontiers in cellular and infection microbiology · 2026Review
- DNA polymerase I is an efficient reverse transcriptase that mediates RNA-templated DNA repair synthesis.bioRxiv : the preprint server for biology · 2025Article
- Torsion is a dynamic regulator of DNA replication stalling and reactivation.Nature communications · 2025Article
- Dual roles of NScience China. Life sciences · 2025Article
117 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Replication-transcription collisions shape genomes, influence evolution, and promote genetic diseases. Although unclear why, head-on transcription (lagging strand genes) is especially disruptive to replication and promotes genomic instability. Here, we find that head-on collisions promote R-loop formation in Bacillus subtilis. We show that pervasive R-loop formation at head-on collision regions completely blocks replication, elevates mutagenesis, and inhibits gene expression. Accordingly, the activity of the R-loop processing enzyme RNase HIII at collision regions is crucial for stress survival in B. subtilis, as many stress response genes are head-on to replication. Remarkably, without RNase HIII, the ability of the intracellular pathogen Listeria monocytogenes to infect and replicate in hosts is weakened significantly, most likely because many virulence genes are head-on to replication. We conclude that the detrimental effects of head-on collisions stem primarily from excessive R-loop formation and that the resolution of these structures is critical for bacterial stress survival and pathogenesis.
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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.