ArticleProceedings of the National Academy of Sciences of the United States of America2015
An underlying mechanism for the increased mutagenesis of lagging-strand genes in Bacillus subtilis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 88 citations in OpenAlex.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- The B. subtilis translesion polymerase Pol Y1 is not strongly recruited to sites of replication upon different types of DNA damage.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
- "ThebioRxiv : 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
- Transcription-Coupled Repair Promotes the Retention of Mutations in Coding Regions During Replication Stress.International journal of molecular sciences · 2026Article
- Mechanisms of chromosomal DNA replication in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2026Review
- The B. subtilis replicative polymerases bind the sliding clamp with different strengths to tune their activity in DNA replication.Nucleic acids research · 2025Article
- Reduced Genetic Heterogeneity for Stable Bioproduction by Harnessing the Bias and Mechanism of Mutation.Microbial biotechnology · 2025Article
- An anti-virulence drug targeting the evolvability protein Mfd protects against infections with antimicrobial resistant ESKAPE pathogens.Nature communications · 2025Article
- Homologous recombination shapes the architecture and evolution of bacterial genomes.Nucleic acids research · 2025Article
- Hallmarks of DNA replication stress responses in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2025Review
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- The translesion polymerase Pol Y1 is a constitutive component of the B. subtilis replication machinery.Nucleic acids research · 2024Article
- Homologous Recombination Shapes the Architecture and Evolution of Bacterial Genomes.bioRxiv : the preprint server for biology · 2024Article
- Article
- A small molecule that inhibits the evolution of antibiotic resistance.NAR molecular medicine · 2024Article
- Mutation bias and adaptation in bacteria.Microbiology (Reading, England) · 2023Review
- RNase H genes cause distinct impacts on RNA:DNA hybrid formation and mutagenesis genome wide.Science advances · 2023Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
We previously reported that lagging-strand genes accumulate mutations faster than those encoded on the leading strand in Bacillus subtilis. Although we proposed that orientation-specific encounters between replication and transcription underlie this phenomenon, the mechanism leading to the increased mutagenesis of lagging-strand genes remained unknown. Here, we report that the transcription-dependent and orientation-specific differences in mutation rates of genes require the B. subtilis Y-family polymerase, PolY1 (yqjH). We find that without PolY1, association of the replicative helicase, DnaC, and the recombination protein, RecA, with lagging-strand genes increases in a transcription-dependent manner. These data suggest that PolY1 promotes efficient replisome progression through lagging-strand genes, thereby reducing potentially detrimental breaks and single-stranded DNA at these loci. Y-family polymerases can alleviate potential obstacles to replisome progression by facilitating DNA lesion bypass, extension of D-loops, or excision repair. We find that the nucleotide excision repair (NER) proteins UvrA, UvrB, and UvrC, but not RecA, are required for transcription-dependent asymmetry in mutation rates of genes in the two orientations. Furthermore, we find that the transcription-coupling repair factor Mfd functions in the same pathway as PolY1 and is also required for increased mutagenesis of lagging-strand genes. Experimental and SNP analyses of B. subtilis genomes show mutational footprints consistent with these findings. We propose that the interplay between replication and transcription increases lesion susceptibility of, specifically, lagging-strand genes, activating an Mfd-dependent error-prone NER mechanism. We propose that this process, at least partially, underlies the accelerated evolution of lagging-strand genes.
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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.