ArticleNature communications2021
Compensatory evolution of Pseudomonas aeruginosa's slow growth phenotype suggests mechanisms of adaptation in cystic fibrosis.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 69 citations in OpenAlex.
- Characterization of two exoUBMC microbiology · 2026Article
- The impact of inoculation methods on bacterial aggregation and antimicrobial susceptibility testing.Microbiology (Reading, England) · 2026Article
- Sublethal Antibiotic Exposure Induces Microevolution of Quinolone Resistance in PathogenicInternational journal of molecular sciences · 2026Article
- Genomic diversity and adaptive resistance mechanisms inmSystems · 2026Article
- Within-host adaptation mutations associated with persistent colonization ofFrontiers in cellular and infection microbiology · 2026Article
- Review
- Time-resolved dual transcriptomics ofBiofilm · 2025Article
- Occurrence of type VI secretion system effector genes in longitudinal isolates ofMicrobial genomics · 2025Article
- Insights on pathoadaptation of sequentialMicrobiology spectrum · 2025Article
- Biofilm Formation ofMicroorganisms · 2025Review
- Co-culture biofilm patterns among different Pseudomonas aeruginosa clones from cystic fibrosis patients.Biofilm · 2025Article
- Diversification ofMicroorganisms · 2025Article
- Genome-wide identification and characterization of stress-responsive genes in Chlorella vulgaris.BMC genomic data · 2025Article
- Pulmonary delivery of excipient-free tobramycin DPIs for the treatment ofFrontiers in pharmacology · 2025Article
- Chronic wounds and adaptiveCurrent research in microbial sciences · 2025Article
- Plasmid-encoded phosphatase RapP enhances cell growth in non-domesticated Bacillus subtilis strains.Nature communications · 2024Article
- Macrolide resistance through uL4 and uL22 ribosomal mutations in Pseudomonas aeruginosa.Nature communications · 2024Article
- Environment-independent distribution of mutational effects emerges from microscopic epistasis.Science (New York, N.Y.) · 2024Article
- Article
- Metabolic specialization drives reduced pathogenicity in Pseudomonas aeruginosa isolates from cystic fibrosis patients.PLoS biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term infection of the airways of cystic fibrosis patients with Pseudomonas aeruginosa is often accompanied by a reduction in bacterial growth rate. This reduction has been hypothesised to increase within-patient fitness and overall persistence of the pathogen. Here, we apply adaptive laboratory evolution to revert the slow growth phenotype of P. aeruginosa clinical strains back to a high growth rate. We identify several evolutionary trajectories and mechanisms leading to fast growth caused by transcriptional and mutational changes, which depend on the stage of adaptation of the strain. Return to high growth rate increases antibiotic susceptibility, which is only partially dependent on reversion of mutations or changes in the transcriptional profile of genes known to be linked to antibiotic resistance. We propose that similar mechanisms and evolutionary trajectories, in reverse direction, may be involved in pathogen adaptation and the establishment of chronic infections in the antibiotic-treated airways of cystic fibrosis patients.
Indexed as
Identifiers
What OpenQuestion holds
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.