ArticlePLoS computational biology2019
Toxin production spontaneously becomes regulated by local cell density in evolving bacterial populations.
Article in PLoS computational biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed.
- Spatial structure: shaping the ecology and evolution of microbial communities.FEMS microbiology reviews · 2026Review
- Dynamic coexistence driven by physiological transitions in microbial communities.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Prevalence, Molecular Characterization, and Antimicrobial Resistance Profile of EnterotoxigenicFoods (Basel, Switzerland) · 2025Article
- Unforeseen current and future benefits of uncommon yeast: the Metschnikowia genus.Applied microbiology and biotechnology · 2024Review
- The Epistemology of Bacterial Virulence Factor Characterization.Microorganisms · 2024Review
- Multiscale selection in spatially structured populations.Proceedings. Biological sciences · 2024Article
- Decolonizing drug-resistantMicrobiology (Reading, England) · 2023Article
- Agent-Based Modeling of Microbial Communities.ACS synthetic biology · 2022Review
- The territorial nature of aggression in biofilms.Frontiers in microbiology · 2022Article
- Community composition of microbial microcosms follows simple assembly rules at evolutionary timescales.Nature communications · 2021Article
- Automated design of synthetic microbial communities.Nature communications · 2021Article
- Experimental Evolution of Interference Competition.Frontiers in microbiology · 2021Article
- Quorum Sensing-Mediated and Growth Phase-Dependent Regulation of Metabolic Pathways inFrontiers in microbiology · 2021Article
- Quorum-Sensing Regulation of Antimicrobial Resistance in Bacteria.Microorganisms · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The production of anticompetitor toxins is widespread among bacteria. Because production of such toxins is costly, it is typically regulated. In particular, many toxins are produced only when the local cell density is high. It is unclear which selection pressures shaped the evolution of density-dependent regulation of toxin production. Here, we study the evolution of toxin production, resistance and the response to a cell-density cue in a model of an evolving bacterial population with spatial structure. We present results for two growth regimes: (i) an undisturbed, fixed habitat in which only small fluctuations of cell density occur, and (ii) a serial-transfer regime with large fluctuations in cell density. We find that density-dependent toxin production can evolve under both regimes. However, the selection pressures driving the evolution of regulation differ. In the fixed habitat, regulation evolves because it allows cells to produce toxin only when opportunities for reproduction are highly limited (because of a high local cell density), and the effective fitness costs of toxin production are hence low. Under serial transfers, regulation evolves because it allows cells to switch from a fast-growing non-toxic phenotype when colonising a new habitat, to a slower-growing competitive toxic phenotype when the cell density increases. Colonies of such regulating cells rapidly expand into unoccupied space because their edges consist of fast-growing, non-toxin-producing cells, but are also combative because cells at the interfaces with competing colonies do produce toxin. Because under the two growth regimes different types of regulation evolve, our results underscore the importance of growth conditions in the evolution of social behaviour in bacteria.
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.