ArticleNature2016
The nature of mutations induced by replication–transcription collisions.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 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.
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Who cites it
99 citing papers in PubMed, 145 citations in OpenAlex.
- Replication-transcription collisions impose DNA strand-specific constraints on gene length in bacteria.PLoS genetics · 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
- Structural principles of transcriptional collisions.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
- Article
- Effect of Mutations on the Evolution of Extended Spectrum β-lactamases (ESBL).The protein journal · 2025Review
- The CGG triplet repeat binding protein 1 counteracts R-loop induced transcription-replication stress.EMBO reports · 2025Article
- GnT Motifs Can Increase T:A→G:C Mutation Rates Over 1000-fold in Bacteria.Molecular biology and evolution · 2025Article
- Update on R-loops in genomic integrity: Formation, functions, and implications for human diseases.Genes & diseases · 2025Review
- Reduced Genetic Heterogeneity for Stable Bioproduction by Harnessing the Bias and Mechanism of Mutation.Microbial biotechnology · 2025Article
- Transcription-replication conflicts drive R-loop-dependent nucleosome eviction and require DOT1L activity for transcription recovery.Nucleic acids research · 2025Article
- An extreme mutational hotspot in nlpD depends on transcriptional induction of rpoS.PLoS genetics · 2025Article
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- Extending evolutionary forecasts across bacterial species.Proceedings. Biological sciences · 2024Article
- Transcription and DNA replication collisions lead to large tandem duplications and expose targetable therapeutic vulnerabilities in cancer.Nature cancer · 2024Article
- The LexA-RecA* structure reveals a cryptic lock-and-key mechanism for SOS activation.Nature structural & molecular biology · 2024Article
- Origin, evolution, and maintenance of gene-strand bias in bacteria.Nucleic acids research · 2024Article
- Transcription as source of genetic heterogeneity in budding yeast.Yeast (Chichester, England) · 2024Review
- Protein lysine four-carbon acylations in health and disease.Journal of cellular physiology · 2024Review
39 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 2 institutions in 1 country.
Funding
Abstract
The DNA replication and transcription machineries share a common DNA template and thus can collide with each other co-directionally or head-on. Replication–transcription collisions can cause replication fork arrest, premature transcription termination, DNA breaks, and recombination intermediates threatening genome integrity. Collisions may also trigger mutations, which are major contributors to genetic disease and evolution. However, the nature and mechanisms of collision-induced mutagenesis remain poorly understood. Here we reveal the genetic consequences of replication–transcription collisions in actively dividing bacteria to be two classes of mutations: duplications/deletions and base substitutions in promoters. Both signatures are highly deleterious but are distinct from the previously well-characterized base substitutions in the coding sequence. Duplications/deletions are probably caused by replication stalling events that are triggered by collisions; their distribution patterns are consistent with where the fork first encounters a transcription complex upon entering a transcription unit. Promoter substitutions result mostly from head-on collisions and frequently occur at a nucleotide that is conserved in promoters recognized by the major σ factor in bacteria. This substitution is generated via adenine deamination on the template strand in the promoter open complex, as a consequence of head-on replication perturbing transcription initiation. We conclude that replication–transcription collisions induce distinct mutation signatures by antagonizing replication and transcription, not only in coding sequences but also in gene regulatory elements.
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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.