ArticleThe Journal of antimicrobial chemotherapy2015
A single nucleotide change in mutY increases the emergence of antibiotic-resistant Campylobacter jejuni mutants.
Article in The Journal of antimicrobial chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- The bile salt deoxycholate inducesFrontiers in microbiology · 2022Article
- Genomic adaptations of Campylobacter jejuni to long-term human colonization.Gut pathogens · 2021Article
- Identification of aFrontiers in microbiology · 2019Article
- Convergent Amino Acid Signatures in Polyphyletic Campylobacter jejuni Subpopulations Suggest Human Niche Tropism.Genome biology and evolution · 2018Article
- A Mutator Phenotype Promoting the Emergence of Spontaneous Oxidative Stress-Resistant Mutants in Campylobacter jejuni.Applied and environmental microbiology · 2017Article
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Authors and funding
5 authors.
Funding
Abstract
objectivesMutator strains play an important role in the emergence of antibiotic-resistant bacteria. Campylobacter jejuni is a leading cause of foodborne illnesses worldwide and is increasingly resistant to clinically important antibiotics. The objective of this study was to identify the genetic basis that contributes to a mutator phenotype in Campylobacter and determine the role of this phenotype in the development of antibiotic resistance.
methodsA C. jejuni isolate (named CMT) showing a mutator phenotype was subjected to WGS analysis. Comparative genomics, site-specific reversion and mutation, and gene knockout were conducted to prove the mutator effect was caused by a single nucleotide change in the mutY gene of C. jejuni.
resultsThe C. jejuni CMT isolate showed ∼ 100-fold higher mutation frequency to ciprofloxacin than the WT strain. Under selection by ciprofloxacin, fluoroquinolone-resistant mutants emerged readily from the CMT isolate. WGS identified a single nucleotide change (G595 → T) in the mutY gene of the CMT isolate. Further experiments using defined mutant constructs proved its specific role in elevating mutation frequencies. The mutY point mutation also led to an ∼ 700-fold increase in the emergence of ampicillin-resistant mutants, indicating its broader impact on antibiotic resistance. Structural modelling suggested the G595 → T mutation probably affects the catalytic domain of MutY and consequently abolishes the anti-mutator function of this DNA repair protein.
conclusionsThe G595 → T mutation in mutY abolishes its anti-mutator function and confers a mutator phenotype in Campylobacter, promoting the emergence of antibiotic-resistant Campylobacter.
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