ArticleAntimicrobial agents and chemotherapy2013
Polymyxin resistance of Pseudomonas aeruginosa phoQ mutants is dependent on additional two-component regulatory systems.
Article in Antimicrobial agents and chemotherapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 131 citations in OpenAlex.
- Transposon insertion sequencing of Pseudomonas aeruginosa identifies multiple intersecting pathways essential for extreme colistin resistance.PLoS pathogens · 2026Article
- Antibiotic resistance mechanisms and global resistance patterns of Pseudomonas aeruginosa in microbial keratitis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- Article
- Distinct proteomic profiles of clinical isolates show diversity of Pseudomonas aeruginosa colistin-resistance.Clinical proteomics · 2026Article
- Colistin Resistance in Bacteria: Current Updates on Mechanism of Action and Combating Strategies.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026Review
- Polymyxin resistance in Gram-negative bacteria: a comprehensive review with a focus on the role of 4-amino-4-doexy-L-arabinose.Molecular biology reports · 2025Review
- The PA2803-encoded PcrP exhibits a novel non-catalytic function and contributes to polymyxin B resistance inJournal of bacteriology · 2025Article
- Metagenome-inspired libraries to engineer phage M13 for targeted killing of Gram-negative bacterial species.Nucleic acids research · 2025Article
- Secreted retropepsin-like enzymes are essential for stress tolerance and biofilm formation inmBio · 2025Article
- The Genetic Background and Culture Medium Only Marginally Affect the In Vitro Evolution ofAntibiotics (Basel, Switzerland) · 2025Article
- Current models in bacterial hemicellulase-encoding gene regulation.Applied microbiology and biotechnology · 2024Review
- Review
- Breaking Barriers: Exploiting Envelope Biogenesis and Stress Responses to Develop Novel Antimicrobial Strategies in Gram-Negative Bacteria.Pathogens (Basel, Switzerland) · 2024Review
- Colistin: Lights and Shadows of an Older Antibiotic.Molecules (Basel, Switzerland) · 2024Review
- Article
- Antimicrobial peptide glatiramer acetate targets Pseudomonas aeruginosa lipopolysaccharides to breach membranes without altering lipopolysaccharide modification.npj antimicrobials and resistance · 2024Article
- Antimicrobial resistance ofFrontiers in microbiology · 2024Review
- Insights into Kinases of ESKAPE Pathogens for Therapeutic Interventions.Cardiovascular & hematological agents in medicinal chemistry · 2024Review
- Polymyxins: recent advances and challenges.Frontiers in pharmacology · 2024Review
- Age of Antibiotic Resistance in MDR/XDR Clinical Pathogen ofPharmaceuticals (Basel, Switzerland) · 2023Review
17 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Pseudomonas aeruginosa can develop resistance to polymyxin as a consequence of mutations in the PhoPQ regulatory system, mediated by covalent lipid A modification. Transposon mutagenesis of a polymyxin-resistant phoQ mutant defined 41 novel loci required for resistance, including two regulatory systems, ColRS and CprRS. Deletion of the colRS genes, individually or in tandem, abrogated the polymyxin resistance of a ΔphoQ mutant, as did individual or tandem deletion of cprRS. Individual deletion of colR or colS in a ΔphoQ mutant also suppressed 4-amino-L-arabinose addition to lipid A, consistent with the known role of this modification in polymyxin resistance. Surprisingly, tandem deletion of colRS or cprRS in the ΔphoQ mutant or individual deletion of cprR or cprS failed to suppress 4-amino-L-arabinose addition to lipid A, indicating that this modification alone is not sufficient for PhoPQ-mediated polymyxin resistance in P. aeruginosa. Episomal expression of colRS or cprRS in tandem or of cprR individually complemented the Pm resistance phenotype in the ΔphoQ mutant, while episomal expression of colR, colS, or cprS individually did not. Highly polymyxin-resistant phoQ mutants of P. aeruginosa isolated from polymyxin-treated cystic fibrosis patients harbored mutant alleles of colRS and cprS; when expressed in a ΔphoQ background, these mutant alleles enhanced polymyxin resistance. These results define ColRS and CprRS as two-component systems regulating polymyxin resistance in P. aeruginosa, indicate that addition of 4-amino-L-arabinose to lipid A is not the only PhoPQ-regulated biochemical mechanism required for resistance, and demonstrate that colRS and cprS mutations can contribute to high-level clinical resistance.
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