ArticleProceedings of the National Academy of Sciences of the United States of America2015
Long-term social dynamics drive loss of function in pathogenic bacteria.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 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
102 citing papers in PubMed, 177 citations in OpenAlex.
- Loss of the ferripyochelin receptor FptA drives reduced cefiderocol susceptibility and impairs fitness inAntimicrobial agents and chemotherapy · 2026Article
- Studying adaptation at the invisible scale.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Occurrence of type VI secretion system effector genes in longitudinal isolates ofMicrobial genomics · 2025Article
- Identification of PilD mutants reveals the iterative social evolution inApplied and environmental microbiology · 2025Article
- Loss of the Ferripyochelin Receptor FptA Drives Reduced Cefiderocol Susceptibility and Impairs Fitness inbioRxiv : the preprint server for biology · 2025Article
- Exploiting social traits for clinical applications in bacteria and viruses.npj antimicrobials and resistance · 2025Review
- Article
- Adaptive evolution of carbapenem-resistant hypervirulentProceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Epistemology of Bacterial Virulence Factor Characterization.Microorganisms · 2024Review
- Secondary metabolite profiling ofmSystems · 2024Article
- Article
- Siderophores promote cooperative interspecies and intraspecies cross-protection against antibiotics in vitro.Nature microbiology · 2024Article
- SOCfinder: a genomic tool for identifying social genes in bacteria.Microbial genomics · 2023Article
- Long-term evolution of antibiotic tolerance inEvolution letters · 2023Article
- Membrane transporters in cell physiology, cancer metabolism and drug response.Disease models & mechanisms · 2023Review
- Article
- Signatures of kin selection in a natural population of the bacteriaEvolution letters · 2023Article
- Equilibria and oscillations in cheat-cooperator dynamics.Evolution letters · 2023Article
- Recombination as an enforcement mechanism of prosocial behavior in cooperating bacteria.iScience · 2023Article
- Within- and between-host dynamics of producer and non-producer pathogens.Parasitology · 2023Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Laboratory experiments show that social interactions between bacterial cells can drive evolutionary change at the population level, but significant challenges limit attempts to assess the relevance of these findings to natural populations, where selection pressures are unknown. We have increasingly sophisticated methods for monitoring phenotypic and genotypic dynamics in bacteria causing infectious disease, but in contrast, we lack evidence-based adaptive explanations for those changes. Evolutionary change during infection is often interpreted as host adaptation, but this assumption neglects to consider social dynamics shown to drive evolutionary change in vitro. We provide evidence to show that long-term behavioral dynamics observed in a pathogen are driven by selection to outcompete neighboring conspecific cells through social interactions. We find that Pseudomonas aeruginosa bacteria, causing lung infections in patients with cystic fibrosis, lose cooperative iron acquisition by siderophore production during infection. This loss could be caused by changes in iron availability in the lung, but surprisingly, we find that cells retain the ability to take up siderophores produced by conspecifics, even after they have lost the ability to synthesize siderophores. Only when cooperative producers are lost from the population is the receptor for uptake lost. This finding highlights the potential pitfalls of interpreting loss of function in pathogenic bacterial populations as evidence for trait redundancy in the host environment. More generally, we provide an example of how sequence analysis can be used to generate testable hypotheses about selection driving long-term phenotypic changes of pathogenic bacteria in situ.
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.