ArticleProceedings of the National Academy of Sciences of the United States of America2011
Impact of a stress-inducible switch to mutagenic repair of DNA breaks on mutation in Escherichia coli.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 126 citations in OpenAlex.
- Targeted protein evolution in the gut microbiome by diversity-generating retroelements.Science (New York, N.Y.) · 2025Article
- A transient mutational burst occurs during yeast colony development.Molecular systems biology · 2025Article
- Antibiotic resistance and preventive strategies in foodborne pathogenic bacteria: a comprehensive review.Food science and biotechnology · 2025Review
- Antibiotic-recalcitrant Salmonella during infection.Nature reviews. Microbiology · 2025Review
- Targeted protein evolution in the gut microbiome by diversity-generating retroelements.bioRxiv : the preprint server for biology · 2024Article
- "Metabolic burden" explained: stress symptoms and its related responses induced by (over)expression of (heterologous) proteins in Escherichia coli.Microbial cell factories · 2024Review
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- Drugging evolution of antibiotic resistance at a regulatory network hub.Science advances · 2023Article
- ppGpp and RNA-polymerase backtracking guide antibiotic-induced mutable gambler cells.Molecular cell · 2023Article
- Resistance-resistant antibacterial treatment strategies.Frontiers in antibiotics · 2023Article
- The rapid evolution of flagellar ion selectivity in experimental populations ofScience advances · 2022Article
- Persisting uropathogenic Escherichia coli lineages show signatures of niche-specific within-host adaptation mediated by mobile genetic elements.Cell host & microbe · 2022Article
- Stress-Induced Mutagenesis, Gambler Cells, and Stealth Targeting Antibiotic-Induced Evolution.mBio · 2022Review
- Identification of a signature of evolutionarily conserved stress-induced mutagenesis in cancer.Frontiers in genetics · 2022Article
- Genotoxic Agents Produce Stressor-Specific Spectra of Spectinomycin Resistance Mutations Based on Mechanism of Action and Selection in Bacillus subtilis.Antimicrobial agents and chemotherapy · 2021Article
- ImuA Facilitates SOS Mutagenesis by Inhibiting RecA-Mediated Activity in Myxococcus xanthus.Applied and environmental microbiology · 2021Article
- Non-Random Genome Editing and Natural Cellular Engineering in Cognition-Based Evolution.Cells · 2021Review
- Single-molecule live-cell imaging reveals RecB-dependent function of DNA polymerase IV in double strand break repair.Nucleic acids research · 2020Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- Selective Inbreeding: Genetic Crosses Drive Apparent Adaptive Mutation in the Cairns-Foster System ofGenetics · 2020Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Basic ideas about the constancy and randomness of mutagenesis that drives evolution were challenged by the discovery of mutation pathways activated by stress responses. These pathways could promote evolution specifically when cells are maladapted to their environment (i.e., are stressed). However, the clearest example--a general stress-response-controlled switch to error-prone DNA break (double-strand break, DSB) repair--was suggested to be peculiar to an Escherichia coli F' conjugative plasmid, not generally significant, and to occur by an alternative stress-independent mechanism. Moreover, mechanisms of spontaneous mutation in E. coli remain obscure. First, we demonstrate that this same mechanism occurs in chromosomes of starving F(-) E. coli. I-SceI endonuclease-induced chromosomal DSBs increase mutation 50-fold, dependent upon general/starvation- and DNA-damage-stress responses, DinB error-prone DNA polymerase, and DSB-repair proteins. Second, DSB repair is also mutagenic if the RpoS general-stress-response activator is expressed in unstressed cells, illustrating a stress-response-controlled switch to mutagenic repair. Third, DSB survival is not improved by RpoS or DinB, indicating that mutagenesis is not an inescapable byproduct of repair. Importantly, fourth, fully half of spontaneous frame-shift and base-substitution mutation during starvation also requires the same stress-response, DSB-repair, and DinB proteins. These data indicate that DSB-repair-dependent stress-induced mutation, driven by spontaneous DNA breaks, is a pathway that cells usually use and a major source of spontaneous mutation. These data also rule out major alternative models for the mechanism. Mechanisms that couple mutagenesis to stress responses can allow cells to evolve rapidly and responsively to their environment.
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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.