ArticleDNA repair2006
Roles of E. coli double-strand-break-repair proteins in stress-induced mutation.
Article in DNA repair, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- Adaptive laboratory evolution of Lactiplantibacillus plantarum enhances furan tolerance and lactic acid production in lignocellulosic hydrolysate.Bioresources and bioprocessing · 2026Article
- The rarA gene as part of an expanded RecFOR recombination pathway: Negative epistasis and synthetic lethality with ruvB, recG, and recQ.PLoS genetics · 2021Article
- Genetic and metabolic signatures of Salmonella enterica subsp. enterica associated with animal sources at the pangenomic scale.BMC genomics · 2019Article
- Selection-Enhanced Mutagenesis ofGenetics · 2018Article
- Characterization of Plasmodium falciparum ATP-dependent DNA helicase RuvB3.Malaria journal · 2016Article
- The Origin of Mutants Under Selection: How Natural Selection Mimics Mutagenesis (Adaptive Mutation).Cold Spring Harbor perspectives in biology · 2015Review
- Stress-Induced Mutagenesis.EcoSal Plus · 2012Article
- Impact of a stress-inducible switch to mutagenic repair of DNA breaks on mutation in Escherichia coli.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Break-induced replication is highly inaccurate.PLoS biology · 2011Article
- The SMC-like protein complex SbcCD enhances DNA polymerase IV-dependent spontaneous mutation in Escherichia coli.Journal of bacteriology · 2011Article
- Separate DNA Pol II- and Pol IV-dependent pathways of stress-induced mutation during double-strand-break repair in Escherichia coli are controlled by RpoS.Journal of bacteriology · 2010Article
- Competition of Escherichia coli DNA polymerases I, II and III with DNA Pol IV in stressed cells.PloS one · 2010Article
- DinB upregulation is the sole role of the SOS response in stress-induced mutagenesis in Escherichia coli.Genetics · 2009Article
- Defects in the error prevention oxidized guanine system potentiate stationary-phase mutagenesis in Bacillus subtilis.Journal of bacteriology · 2009Article
- Hypermutability of damaged single-strand DNA formed at double-strand breaks and uncapped telomeres in yeast Saccharomyces cerevisiae.PLoS genetics · 2008Article
- Endogenous oxidative stress produces diversity and adaptability in biofilm communities.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Novel role of mfd: effects on stationary-phase mutagenesis in Bacillus subtilis.Journal of bacteriology · 2006Article
- Single-strand-specific exonucleases prevent frameshift mutagenesis by suppressing SOS induction and the action of DinB/DNA polymerase IV in growing cells.Journal of bacteriology · 2006Article
- Mutation as a stress response and the regulation of evolvability.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Special mechanisms of mutation are induced during growth-limiting stress and can generate adaptive mutations that permit growth. These mechanisms may provide improved models for mutagenesis in antibiotic resistance, evolution of pathogens, cancer progression and chemotherapy resistance. Stress-induced reversion of an Escherichia coli episomal lac frameshift allele specifically requires DNA double-strand-break-repair (DSBR) proteins, the SOS DNA-damage response and its error-prone DNA polymerase, DinB. We distinguished two possible roles for the DSBR proteins. Each might act solely upstream of SOS, to create single-strand DNA that induces SOS. This could upregulate DinB and enhance mutation globally. Or any or all of them might function other than or in addition to SOS promotion, for example, directly in error-prone DSBR. We report that in cells with SOS genes derepressed constitutively, RecA, RuvA, RuvB, RuvC, RecF, and TraI remain required for stress-induced mutation, demonstrating that these proteins act other than via SOS induction. RecA and TraI also act by promoting SOS. These and additional results with hyper-mutating recD and recG mutants support roles for these proteins via error-prone DSBR. Such mechanisms could localize stress-induced mutagenesis to small genomic regions, a potentially important strategy for adaptive evolution, both for reducing additional deleterious mutations in rare adaptive mutants and for concerted evolution of genes.
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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.