ArticlePLoS genetics2008
Mutability and importance of a hypermutable cell subpopulation that produces stress-induced mutants in Escherichia coli.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 56 citations in OpenAlex.
- Growth rate-dependent mutations and phenotypic switching facilitate rapid adaptation.NPJ systems biology and applications · 2026Article
- Stress-Induced Mutagenesis, Gambler Cells, and Stealth Targeting Antibiotic-Induced Evolution.mBio · 2022Review
- Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes.Cancers · 2019Review
- Evolution of Resistance in Cancer: A Cell Cycle Perspective.Frontiers in oncology · 2019Review
- Oxygen and RNA in stress-induced mutation.Current genetics · 2018Review
- Real-time dynamics of mutagenesis reveal the chronology of DNA repair and damage tolerance responses in single cells.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Stress-Induced Mutagenesis: Implications in Cancer and Drug Resistance.Annual review of cancer biology · 2017Article
- Role of Ribonucleotide Reductase in Bacillus subtilis Stress-Associated Mutagenesis.Journal of bacteriology · 2017Article
- Population Heterogeneity in Mutation Rate Increases the Frequency of Higher-Order Mutants and Reduces Long-Term Mutational Load.Molecular biology and evolution · 2017Article
- Phenotypic heterogeneity in a bacteriophage population only appears as stress-induced mutagenesis.Current genetics · 2016Review
- Single-Cell Analysis of RNA Virus Infection Identifies Multiple Genetically Diverse Viral Genomes within Single Infectious Units.Cell host & microbe · 2015Article
- Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
- Starvation induces phenotypic diversification and convergent evolution in Vibrio vulnificus.PloS one · 2014Article
- Elevated mutagenesis does not explain the increased frequency of antibiotic resistant mutants in starved aging colonies.PLoS genetics · 2013Article
- A strategically located serine residue is critical for the mutator activity of DNA polymerase IV from Escherichia coli.Nucleic acids research · 2013Article
- Evaluating evolutionary models of stress-induced mutagenesis in bacteria.Nature reviews. Genetics · 2013Review
- Starvation-associated genome restructuring can lead to reproductive isolation in yeast.PloS one · 2013Article
- Stress-Induced Mutagenesis.EcoSal Plus · 2012Article
- Stress-induced mutation via DNA breaks in Escherichia coli: a molecular mechanism with implications for evolution and medicine.BioEssays : news and reviews in molecular, cellular and developmental biology · 2012Article
- The TCA cycle is not required for selection or survival of multidrug-resistant Salmonella.The Journal of antimicrobial chemotherapy · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
In bacterial, yeast, and human cells, stress-induced mutation mechanisms are induced in growth-limiting environments and produce non-adaptive and adaptive mutations. These mechanisms may accelerate evolution specifically when cells are maladapted to their environments, i.e., when they are are stressed. One mechanism of stress-induced mutagenesis in Escherichia coli occurs by error-prone DNA double-strand break (DSB) repair. This mechanism was linked previously to a differentiated subpopulation of cells with a transiently elevated mutation rate, a hypermutable cell subpopulation (HMS). The HMS could be important, producing essentially all stress-induced mutants. Alternatively, the HMS was proposed to produce only a minority of stress-induced mutants, i.e., it was proposed to be peripheral. We characterize three aspects of the HMS. First, using improved mutation-detection methods, we estimate the number of mutations per genome of HMS-derived cells and find that it is compatible with fitness after the HMS state. This implies that these mutants are not necessarily an evolutionary dead end, and could contribute to adaptive evolution. Second, we show that stress-induced Lac(+) mutants, with and without evidence of descent from the HMS, have similar Lac(+) mutation sequences. This provides evidence that HMS-descended and most stress-induced mutants form via a common mechanism. Third, mutation-stimulating DSBs introduced via I-SceI endonuclease in vivo do not promote Lac(+) mutation independently of the HMS. This and the previous finding support the hypothesis that the HMS underlies most stress-induced mutants, not just a minority of them, i.e., it is important. We consider a model in which HMS differentiation is controlled by stress responses. Differentiation of an HMS potentially limits the risks of mutagenesis in cell clones.
Indexed as
Identifiers
What OpenQuestion holds
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.