ArticleGenetics2004
General stress response regulator RpoS in adaptive mutation and amplification in Escherichia coli.
Article in Genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 138 citations in OpenAlex.
- Growth rate-dependent mutations and phenotypic switching facilitate rapid adaptation.NPJ systems biology and applications · 2026Article
- Resisting the gallium "Trojan horse": Experimental evolutionary insights into microbial resistance.Gene & protein in disease · 2026Article
- Alternative nucleic acid structures in microbial biology: regulatory functions and antimicrobial opportunities.Frontiers in cellular and infection microbiology · 2026Review
- Simulated microgravity triggers a membrane adaptation to stress in E. coli REL606.BMC microbiology · 2025Article
- Gallium Resistance inApplied microbiology (Basel, Switzerland) · 2025Article
- Modeling stress-induced responses: plasticity in continuous state space and gradual clonal evolution.Theory in biosciences = Theorie in den Biowissenschaften · 2024Article
- A three-colour stress biosensor reveals multimodal response in single cells and spatiotemporal dynamics of biofilms.NPJ biofilms and microbiomes · 2023Article
- 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
- Minireview: Engineering evolution to reconfigure phenotypic traits in microbes for biotechnological applications.Computational and structural biotechnology journal · 2023Review
- Stress-Induced Mutagenesis, Gambler Cells, and Stealth Targeting Antibiotic-Induced Evolution.mBio · 2022Review
- Selective Inbreeding: Genetic Crosses Drive Apparent Adaptive Mutation in the Cairns-Foster System ofGenetics · 2020Article
- Transcriptomic Basis of Serum Resistance and Virulence Related Traits in XDRFrontiers in microbiology · 2020Article
- Gamblers: An Antibiotic-Induced Evolvable Cell Subpopulation Differentiated by Reactive-Oxygen-Induced General Stress Response.Molecular cell · 2019Article
- Selection and Plasmid Transfer Underlie Adaptive Mutation inGenetics · 2018Article
- Fungal Resistance to Echinocandins and the MDR Phenomenon inJournal of fungi (Basel, Switzerland) · 2018Review
- Oxygen and RNA in stress-induced mutation.Current genetics · 2018Review
- Selection-Enhanced Mutagenesis ofGenetics · 2018Article
- Persistent damaged bases in DNA allow mutagenic break repair in Escherichia coli.PLoS genetics · 2017Article
- Stress-Induced Mutagenesis: Implications in Cancer and Drug Resistance.Annual review of cancer biology · 2017Article
24 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Microbial cells under growth-limiting stress can generate mutations by mechanisms distinct from those in rapidly growing cells. These mechanisms might be specific stress responses that increase mutation rates, potentially altering rates of evolution, or might reflect non-stress-specific processes in rare growing cells. In an Escherichia coli model system, both frameshift reversion mutations and gene amplifications occur as apparent starvation-induced mutations. Whereas frameshift reversion ("point mutation") requires recombination proteins, the SOS response, and error-prone DNA polymerase IV (DinB), amplification requires neither SOS nor pol IV. We report that both point mutation and amplification require the stationary-phase and general stress response transcription factor RpoS (sigmaS). Growth-dependent mutation does not. Alternative interpretations are excluded. The results imply, first, that point mutation and amplification are stress responses that occur in differentiated stationary-phase (not rare growing) cells and, second, that transient genetic instability, producing both point mutation and genome rearrangement, may be a previously unrecognized component of the RpoS-dependent general stress response.
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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.