ArticleJournal of molecular biology2017
RNase HII Saves rnhA Mutant Escherichia coli from R-Loop-Associated Chromosomal Fragmentation.
Article in Journal of molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Synthetic lethal mutants inJournal of bacteriology · 2023Pooled it
- DNA polymerase I and DnaE mediate RNA-templated DNA synthesis over embedded ribonucleotides.Nucleic acids research · 2026Article
- Ribonucleotide errors, RNase HII, and ribonucleotide excision repair.Critical reviews in biochemistry and molecular biology · 2026Review
- Processing of reversed replication forks is required for the resolution of replication-transcription conflicts.Nucleic acids research · 2026Article
- DNA polymerase I: structure, activity, and function in bacterial DNA replication and repair.Critical reviews in biochemistry and molecular biology · 2026Review
- Tripleknock: predicting lethal effect of three-gene knockout in bacteria by deep learning.Scientific reports · 2026Article
- Bacillus subtilis RNase HII Is Inefficient at Processing Guanosine Monophosphate and Damaged Ribonucleotides.Molecular microbiology · 2026Article
- Genomes of NBMC genomics · 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
- Genome-wide ribonucleotide detection in Archaea.Nucleic acids research · 2025Article
- Article
- The bacterial transcription terminator, Rho, functions as an RNA:DNA hybrid (RDH) helicase in vivo.The Biochemical journal · 2025Article
- UV induces codirectional replication-transcription conflicts and an alternative DnaA-dependent replication origin in the rnhAB mutants of Escherichiacoli.Nucleic acids research · 2025Article
- Escherichia coli DNA replication: the old model organism still holds many surprises.FEMS microbiology reviews · 2024Review
- RNase H genes cause distinct impacts on RNA:DNA hybrid formation and mutagenesis genome wide.Science advances · 2023Article
- Human PNPase causes RNA stabilization and accumulation of R-loops in the Escherichia coli model system.Scientific reports · 2023Article
- RNase H genes cause distinct impacts on RNA:DNA hybrid formation and mutagenesis genome-wide.bioRxiv : the preprint server for biology · 2023Article
- Strand specificity of ribonucleotide excision repair in Escherichia coli.Nucleic acids research · 2023Article
- Robust linear DNA degradation supports replication-initiation-defective mutants in Escherichia coli.G3 (Bethesda, Md.) · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The rnhAB mutant Escherichia coli, deficient in two RNase H enzymes that remove both R-loops and incorporated ribonucleotides (rNs) from DNA, grow slowly, suggesting accumulation of rN-containing DNA lesions (R-lesions). We report that the rnhAB mutants have reduced viability, form filaments with abnormal nucleoids, induce SOS, and fragment their chromosome, revealing replication and/or segregation stress. R-loops are known to interfere with replication forks, and sensitivity of the double rnhAB mutants to translation inhibition points to R-loops as precursors for R-lesions. However, the strict specificity of bacterial RNase HII for RNA-DNA junctions indicates that R-lesions have rNs integrated into DNA. Indeed, instead of relieving problems of rnhAB mutants, transient inhibition of replication from oriC kills them, suggesting that oriC-initiated replication removes R-loops instead of compounding them to R-lesions. Yet, replication from an R-loop-initiating plasmid origin kills the double rnhAB mutant, revealing generation of R-lesions by R-loop-primed DNA synthesis. These R-lesions could be R-tracts, contiguous runs of ≥4 RNA nucleotides within DNA strand and the only common substrate between the two bacterial RNase H enzymes. However, a plasmid relaxation test failed to detect R-tracts in DNA of the rnhAB mutants, although it readily detected R-patches (runs of 1-3 rNs). Instead, we detected R-gaps, single-strand gaps containing rNs, in the chromosomal DNA of the rnhAB mutant. Therefore, we propose that RNase H-deficient mutants convert some R-loops into R-tracts, which progress into R-gaps and then to double-strand breaks-explaining why R-tracts do not accumulate in RNase H-deficient cells, while double-strand breaks do.
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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.