ArticleJournal of bacteriology2016
The Small RNA GcvB Promotes Mutagenic Break Repair by Opposing the Membrane Stress Response.
Article in Journal of bacteriology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
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.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- From Environmental Persistence to Host Adaptation: Differential Curli Regulation inMicroorganisms · 2026Review
- Article
- Tiny but Mighty: Small RNAs-The Micromanagers of Bacterial Survival, Virulence, and Host-Pathogen Interactions.Non-coding RNA · 2025Review
- The global RNA-RNA interactome ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Drugging evolution of antibiotic resistance at a regulatory network hub.Science advances · 2023Article
- Small RNA GcvB Regulates Oxidative Stress Response ofAntioxidants (Basel, Switzerland) · 2021Article
- Crucial Role of the C-Terminal Domain of Hfq Protein in Genomic Instability.Microorganisms · 2020Article
- Targeting Hsp20 Using the Novel Small Non-coding RNAFrontiers in microbiology · 2019Article
- Polynucleotide phosphorylase: Not merely an RNase but a pivotal post-transcriptional regulator.PLoS genetics · 2018Review
- Small Regulatory RNAs in the Enterobacterial Response to Envelope Damage and Oxidative Stress.Microbiology spectrum · 2018Review
- Errors in mutagenesis and the benefit of cell-to-cell signalling in the evolution of stress-induced mutagenesis.Royal Society open science · 2017Article
- Hfq links translation repression to stress-induced mutagenesis inGenes & development · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Microbes and human cells possess mechanisms of mutagenesis activated by stress responses. Stress-inducible mutagenesis mechanisms may provide important models for mutagenesis that drives host-pathogen interactions, antibiotic resistance, and possibly much of evolution generally. In Escherichia coli, repair of DNA double-strand breaks is switched to a mutagenic mode, using error-prone DNA polymerases, via the SOS DNA damage and general (σ IMPORTANCE: Mutagenesis mechanisms upregulated by stress responses promote de novo antibiotic resistance and cross-resistance in bacteria, antifungal drug resistance in yeasts, and genome instability in cancer cells under hypoxic stress. This paper describes the role of a small RNA (sRNA) in promoting a stress-inducible-mutagenesis mechanism, mutagenic DNA break repair in Escherichia coli The roles of many sRNAs in E. coli remain unknown. This study shows that ΔgcvB cells, which lack the GcvB sRNA, display a hyperactivated membrane stress response and reduced general stress response, possibly because of sigma factor competition for RNA polymerase. This results in a mutagenic break repair defect. The data illuminate a function of GcvB sRNA in opposing the membrane stress response, and thus indirectly upregulating mutagenesis.
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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.