ArticleAntimicrobial agents and chemotherapy2000
Non-target gene mutations in the development of fluoroquinolone resistance in Escherichia coli.
Article in Antimicrobial agents and chemotherapy, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 143 citations in OpenAlex.
- Strain-dependent contribution of the AcrAB-TolC efflux pump toMicrobiology (Reading, England) · 2025Article
- Tazobactam selects for multidrug resistance.npj antimicrobials and resistance · 2025Article
- Antibiotic-induced stress responses in Gram-negative bacteria and their role in antibiotic resistance.The Journal of antimicrobial chemotherapy · 2025Review
- Fluoroquinolone-specific resistance trajectories in E. coli and their dependence on the SOS-response.BMC microbiology · 2025Article
- Flumequine, a fluoroquinolone in disguise.npj antimicrobials and resistance · 2024Article
- Comparative reassessment of AcrB efflux inhibitors reveals differential impact of specific pump mutations on the activity of potent compounds.Microbiology spectrum · 2024Article
- Genomic Characterization and Genetic Profiles ofGenes · 2023Article
- Genome-wide analysis of genes involved in efflux function and regulation withinMicrobiology (Reading, England) · 2023Article
- Article
- Exploring the Contribution of the AcrB Homolog MdtF to Drug Resistance and Dye Efflux in a Multidrug ResistantAntibiotics (Basel, Switzerland) · 2021Article
- Limited Multidrug Resistance Efflux Pump Overexpression among Multidrug-Resistant Escherichia coli Strains of ST131.Antimicrobial agents and chemotherapy · 2021Article
- New Topoisomerase Inhibitors: Evaluating the Potency of Gepotidacin and Zoliflodacin in Fluoroquinolone-Resistant Escherichia coli uponAntimicrobial agents and chemotherapy · 2021Article
- Quinolones: Mechanism, Lethality and Their Contributions to Antibiotic Resistance.Molecules (Basel, Switzerland) · 2020Review
- Development and selection of low-level multi-drug resistance over an extended range of sub-inhibitory ciprofloxacin concentrations in Escherichia coli.Scientific reports · 2020Article
- MarA, RamA, and SoxS as Mediators of the Stress Response: Survival at a Cost.Frontiers in microbiology · 2020Article
- Comparative Genome Analyses of Wild Type- and Quinolone ResistantFrontiers in microbiology · 2020Article
- Dissecting the molecular evolution of fluoroquinolone-resistant Shigella sonnei.Nature communications · 2019Article
- Efflux-Mediated Resistance to New Oxazolidinones and Pleuromutilin Derivatives in Escherichia coli with Class Specificities in the Resistance-Nodulation-Cell Division-Type Drug Transport Pathways.Antimicrobial agents and chemotherapy · 2019Article
- Proof of an Outer Membrane Target of the Efflux Inhibitor Phe-Arg-β-Naphthylamide from Random Mutagenesis.Molecules (Basel, Switzerland) · 2019Article
- Conserved collateral antibiotic susceptibility networks in diverse clinical strains of Escherichia coli.Nature communications · 2018Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in loci other than genes for the target topoisomerases of fluoroquinolones, gyrA and parC, may play a role in the development of fluoroquinolone resistance in Escherichia coli. A series of mutants with increasing resistance to ofloxacin was obtained from an E. coli K-12 strain and five clinical isolates. First-step mutants acquired a gyrA mutation. Second-step mutants reproducibly acquired a phenotype of multiple antibiotic resistance (Mar) and organic solvent tolerance and showed enhanced fluoroquinolone efflux. None of the second-step mutants showed additional topoisomerase mutations. All second-step mutants showed constitutive expression of marA and/or overexpressed soxS. In some third-step mutants, fluoroquinolone efflux was further enhanced compared to that for second-step mutants, even when the mutant had acquired additional topoisomerase mutations. Attempts to circumvent the second-step Mar mutation by induction of the mar locus with sodium salicylate and thus to select for pure topoisomerase mutants at the second step were not successful. At least in vitro, non-target gene mutations accumulate in second- and third-step mutants upon exposure to a fluoroquinolone and typically include, but do not appear to be limited to, mutations in the mar or sox regulons with consequent increased drug efflux.
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