ArticleAntimicrobial agents and chemotherapy2012
Determinants of intrinsic aminoglycoside resistance in Pseudomonas aeruginosa.
Article in Antimicrobial agents and chemotherapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 65 citations in OpenAlex.
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- Common regulatory mutation increases single-cell survival to antibiotic exposures inbioRxiv : the preprint server for biology · 2024Article
- Antibiotic influx and efflux in Pseudomonas aeruginosa: Regulation and therapeutic implications.Microbial biotechnology · 2024Review
- The Pseudomonas aeruginosa Resistome: Permanent and Transient Antibiotic Resistance, an Overview.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The Inactivation of the Putative Two-Component System Sensor PA14_27940 Increases the Susceptibility to Several Antibiotics and Reduces the Motility ofInternational journal of molecular sciences · 2023Article
- Gene-Gene Interactions Reduce Aminoglycoside Susceptibility ofAntibiotics (Basel, Switzerland) · 2023Article
- A Single Amino Acid Substitution in Elongation Factor G Can Confer Low-Level Gentamicin Resistance inAntimicrobial agents and chemotherapy · 2022Article
- Antibiotic Combination Therapy: A Strategy to Overcome Bacterial Resistance to Aminoglycoside Antibiotics.Frontiers in pharmacology · 2022Review
- The predictive potential of different molecular markers linked to amikacin susceptibility phenotypes in Pseudomonas aeruginosa.PloS one · 2022Article
- Common recognition topology of mex transporters ofFrontiers in pharmacology · 2022Article
- Antibiotic Resistance in Pseudomonas.Advances in experimental medicine and biology · 2022Article
- Genome evolution drives transcriptomic and phenotypic adaptation inMicrobial genomics · 2021Article
- Antibiotic resistance: Time of synthesis in a post-genomic age.Computational and structural biotechnology journal · 2021Review
- Analysis of theAntimicrobial agents and chemotherapy · 2019Article
- Host metabolites stimulate the bacterial proton motive force to enhance the activity of aminoglycoside antibiotics.PLoS pathogens · 2019Article
- Characterization of the diverse plasmid pool harbored by the blaNDM-1-containing Acinetobacter bereziniae HPC229 clinical strain.PloS one · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Screening of a transposon insertion mutant library of Pseudomonas aeruginosa for increased susceptibility to paromomycin identified a number of genes whose disruption enhanced susceptibility of this organism to multiple aminoglycosides, including tobramycin, amikacin, and gentamicin. These included genes associated with lipid biosynthesis or metabolism (lptA, faoA), phosphate uptake (pstB), and two-component regulators (amgRS, PA2797-PA2798) and a gene of unknown function (PA0392). Deletion mutants lacking these showed enhanced panaminoglycoside susceptibility that was reversed by the cloned genes, confirming their contribution to intrinsic panaminoglycoside resistance. None of these mutants showed increased aminoglycoside permeation of the cell envelope, indicating that increased susceptibility was not related to enhanced aminoglycoside uptake owing to a reduced envelope barrier function. Several mutants (pstB, faoA, PA0392, amgR) did, however, show increased cytoplasmic membrane depolarization relative to wild type following gentamicin exposure, consistent with the membranes of these mutants being more prone to perturbation, likely by gentamicin-generated mistranslated polypeptides. Mutants lacking any two of these resistance genes in various combinations invariably showed increased aminoglycoside susceptibility relative to single-deletion mutants, confirming their independent contribution to resistance and highlighting the complexity of the intrinsic aminoglycoside resistome in P. aeruginosa. Deletion of these genes also compromised the high-level panaminoglycoside resistance of clinical isolates, emphasizing their important contribution to acquired resistance.
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