ArticleNature communications2016
The evolution of antimicrobial peptide resistance in Pseudomonas aeruginosa is shaped by strong epistatic interactions.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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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Who cites it
85 citing papers in PubMed, 150 citations in OpenAlex.
- Smaller Genomes and Shorter Prophage Sequences Differentiate Clinical from Environmental Isolates ofbioRxiv : the preprint server for biology · 2026Article
- Transposon insertion sequencing of Pseudomonas aeruginosa identifies multiple intersecting pathways essential for extreme colistin resistance.PLoS pathogens · 2026Article
- Modulation of rob expression accelerates development of antibiotic resistance in Yersinia enterocolitica.Nucleic acids research · 2026Article
- Resistance potentiators: Evolutionary catalysts of antibiotic resistance.PLoS biology · 2026Article
- Role of antimicrobial peptide-based biomaterials in respiratory tract infections control.BMC microbiology · 2026Review
- Design of Multifunctional Bioactive Peptides for Potential Application in Food Packaging: A Machine-Learning-Integrated Optimization Framework.ACS omega · 2026Article
- Antimicrobial peptides: An important link in the game theory between plants and pathogens.Journal of advanced research · 2026Review
- Direct interaction between phosphotransferase LpxT and ArnT modulates polymyxin B resistance inMicrobiology spectrum · 2026Article
- Distinct proteomic profiles of clinical isolates show diversity of Pseudomonas aeruginosa colistin-resistance.Clinical proteomics · 2026Article
- Molecular characteristics of chromosome-mediated colistin resistance in carbapenem-resistant Pseudomonas aeruginosa isolates from a tertiary hospital in China.BMC microbiology · 2026Article
- Evolutionary drivers of divergent collateral sensitivity responses during antibiotic therapy.Nature ecology & evolution · 2026Review
- Magnesium depletion by Candida albicans unleashes two unusual modes of colistin resistance in Pseudomonas aeruginosa with different fitness costs.PLoS biology · 2026Article
- ThemBio · 2026Article
- Macrolide resistance trajectories across threeFrontiers in microbiology · 2026Article
- An intracellular release peptide display technology unveils an antimicrobial peptide with low probability for resistance development.iScience · 2025Article
- Uncovering the genetic basis ofiScience · 2025Article
- The Genetic Background and Culture Medium Only Marginally Affect the In Vitro Evolution ofAntibiotics (Basel, Switzerland) · 2025Article
- Contact Lens Wear Alters Transcriptional Responses to Pseudomonas aeruginosa in Both the Corneal Epithelium and the Bacteria.Investigative ophthalmology & visual science · 2025Article
- Mutational signature analysis predicts bacterial hypermutation and multidrug resistance.Nature communications · 2025Article
- Protein functional domain analysis enhances genotype-phenotype associations in comparative genomic studies ofFrontiers in microbiology · 2025Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colistin is an antimicrobial peptide that has become the only remaining alternative for the treatment of multidrug-resistant Gram-negative bacterial infections, but little is known of how clinical levels of colistin resistance evolve. We use in vitro experimental evolution and whole-genome sequencing of colistin-resistant Pseudomonas aeruginosa isolates from cystic fibrosis patients to reconstruct the molecular evolutionary pathways open for high-level colistin resistance. We show that the evolution of resistance is a complex, multistep process that requires mutation in at least five independent loci that synergistically create the phenotype. Strong intergenic epistasis limits the number of possible evolutionary pathways to resistance. Mutations in transcriptional regulators are essential for resistance evolution and function as nodes that potentiate further evolution towards higher resistance by functionalizing and increasing the effect of the other mutations. These results add to our understanding of clinical antimicrobial peptide resistance and the prediction of resistance evolution.
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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.