ArticlePloS one2011
Epistatic roles for Pseudomonas aeruginosa MutS and DinB (DNA Pol IV) in coping with reactive oxygen species-induced DNA damage.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Cationic antimicrobial peptides promote microbial mutagenesis and pathoadaptation in chronic infections.PLoS pathogens · 2014Trial
- The low-fidelity DNA Pol IV accelerates evolution of pathogenicity genes in Pseudomonas aeruginosa.Communications biology · 2025Article
- Mutational signature analysis predicts bacterial hypermutation and multidrug resistance.Nature communications · 2025Article
- RecA and Specialized Error-Prone DNA Polymerases Are Not Required for Mutagenesis and Antibiotic Resistance Induced by Fluoroquinolones inAntibiotics (Basel, Switzerland) · 2022Article
- The methylation-independent mismatch repair machinery inMicrobiology (Reading, England) · 2021Review
- The Mutant βJournal of bacteriology · 2021Article
- Cystic Fibrosis and Pseudomonas aeruginosa: the Host-Microbe Interface.Clinical microbiology reviews · 2019Review
- Nutrient reduction induced stringent responses promote bacterial quorum-sensing divergence for population fitness.Scientific reports · 2016Article
- Optimization of Polymyxin B in Combination with Doripenem To Combat Mutator Pseudomonas aeruginosa.Antimicrobial agents and chemotherapy · 2016Article
- The sliding clamp tethers the endonuclease domain of MutL to DNA.Nucleic acids research · 2015Article
- A Genetic Selection for dinB Mutants Reveals an Interaction between DNA Polymerase IV and the Replicative Polymerase That Is Required for Translesion Synthesis.PLoS genetics · 2015Article
- Emergence of polymyxin B resistance influences pathogenicity in Pseudomonas aeruginosa mutators.Antimicrobial agents and chemotherapy · 2015Article
- Article
- Pharmacokinetics and pharmacodynamics of aerosolized antibacterial agents in chronically infected cystic fibrosis patients.Clinical microbiology reviews · 2014Review
- The Pseudomonas aeruginosa AlgZR two-component system coordinates multiple phenotypes.Frontiers in cellular and infection microbiology · 2014Review
- A trade-off between oxidative stress resistance and DNA repair plays a role in the evolution of elevated mutation rates in bacteria.Proceedings. Biological sciences · 2013Article
- Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Pseudomonas aeruginosa is especially adept at colonizing the airways of individuals afflicted with the autosomal recessive disease cystic fibrosis (CF). CF patients suffer from chronic airway inflammation, which contributes to lung deterioration. Once established in the airways, P. aeruginosa continuously adapts to the changing environment, in part through acquisition of beneficial mutations via a process termed pathoadaptation. MutS and DinB are proposed to play opposing roles in P. aeruginosa pathoadaptation: MutS acts in replication-coupled mismatch repair, which acts to limit spontaneous mutations; in contrast, DinB (DNA polymerase IV) catalyzes error-prone bypass of DNA lesions, contributing to mutations. As part of an ongoing effort to understand mechanisms underlying P. aeruginosa pathoadaptation, we characterized hydrogen peroxide (H(2)O(2))-induced phenotypes of isogenic P. aeruginosa strains bearing different combinations of mutS and dinB alleles. Our results demonstrate an unexpected epistatic relationship between mutS and dinB with respect to H(2)O(2)-induced cell killing involving error-prone repair and/or tolerance of oxidized DNA lesions. In striking contrast to these error-prone roles, both MutS and DinB played largely accurate roles in coping with DNA lesions induced by ultraviolet light, mitomycin C, or 4-nitroquinilone 1-oxide. Models discussing roles for MutS and DinB functionality in DNA damage-induced mutagenesis, particularly during CF airway colonization and subsequent P. aeruginosa pathoadaptation are discussed.
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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.