ArticleGenetics2009
DinB upregulation is the sole role of the SOS response in stress-induced mutagenesis in Escherichia coli.
Article in Genetics, 2009. 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, 116 citations in OpenAlex.
- Growth rate-dependent mutations and phenotypic switching facilitate rapid adaptation.NPJ systems biology and applications · 2026Article
- On the role of dcm and vsr in Escherichia coli adaptive mutation.Molecular genetics and genomics : MGG · 2025Article
- Core Perturbomes ofPathogens (Basel, Switzerland) · 2025Article
- Snapshots ofiScience · 2025Article
- Stress-resistant but phage-sensitive host mutants induced by phage T4 ghost adsorption.Frontiers in microbiology · 2025Article
- Genetic adaptation to amoxicillin in Escherichia coli: The limited role of dinB and katE.PloS one · 2025Article
- Modeling stress-induced responses: plasticity in continuous state space and gradual clonal evolution.Theory in biosciences = Theorie in den Biowissenschaften · 2024Article
- Mechanisms underlying the low-temperature adaptation of 17β-estradiol-degrading bacterial strainFrontiers in microbiology · 2024Article
- Synergistic Effect of SOS Response and GATC Methylome Suppression on Antibiotic Stress Survival in Escherichia coli.Antimicrobial agents and chemotherapy · 2023Article
- Ampicillin-controlled glucose metabolism manipulates the transition from tolerance to resistance in bacteria.Science advances · 2023Article
- Stress-Induced Mutagenesis, Gambler Cells, and Stealth Targeting Antibiotic-Induced Evolution.mBio · 2022Review
- Exploration of inhibitors of the bacterial LexA repressor-protease.Bioorganic & medicinal chemistry letters · 2022Article
- Sending out an SOS - the bacterial DNA damage response.Genetics and molecular biology · 2022Article
- Potentiating antibiotic efficacy via perturbation of non-essential gene expression.Communications biology · 2021Article
- Quantifying the optimal strategy of population control of quorum sensing network in Escherichia coli.NPJ systems biology and applications · 2021Article
- Effect of mismatch repair on the mutational footprint of the bacterial SOS mutator activity.DNA repair · 2021Article
- Effect of arsenite and growth in biofilm conditions on the evolution ofMicrobial genomics · 2020Article
- Regulation of the error-prone DNA polymerase Polκ by oncogenic signaling and its contribution to drug resistance.Science signaling · 2020Article
- Yeast Spontaneous Mutation Rate and Spectrum Vary with Environment.Current biology : CB · 2019Article
- What is mutation? A chapter in the series: How microbes "jeopardize" the modern synthesis.PLoS genetics · 2019Review
14 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
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Stress-induced mutagenesis is a collection of mechanisms observed in bacterial, yeast, and human cells in which adverse conditions provoke mutagenesis, often under the control of stress responses. Control of mutagenesis by stress responses may accelerate evolution specifically when cells are maladapted to their environments, i.e., are stressed. It is therefore important to understand how stress responses increase mutagenesis. In the Escherichia coli Lac assay, stress-induced point mutagenesis requires induction of at least two stress responses: the RpoS-controlled general/starvation stress response and the SOS DNA-damage response, both of which upregulate DinB error-prone DNA polymerase, among other genes required for Lac mutagenesis. We show that upregulation of DinB is the only aspect of the SOS response needed for stress-induced mutagenesis. We constructed two dinB(o(c)) (operator-constitutive) mutants. Both produce SOS-induced levels of DinB constitutively. We find that both dinB(o(c)) alleles fully suppress the phenotype of constitutively SOS-"off" lexA(Ind(-)) mutant cells, restoring normal levels of stress-induced mutagenesis. Thus, dinB is the only SOS gene required at induced levels for stress-induced point mutagenesis. Furthermore, although spontaneous SOS induction has been observed to occur in only a small fraction of cells, upregulation of dinB by the dinB(o(c)) alleles in all cells does not promote a further increase in mutagenesis, implying that SOS induction of DinB, although necessary, is insufficient to differentiate cells into a hypermutable condition.
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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.