Evidence map›Paper›PMID 34555011›Full record

ArticlePLoS computational biology2021

Phenotypic-dependent variability and the emergence of tolerance in bacterial populations.

José Camacho Mateu, Matteo Sireci, Miguel A Muñoz

Abstract read
In one paragraph

Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Frontiers in cellular and infection microbiology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

José Camacho MateuDepartamento de Matemáticas, Universidad Carlos III de Madrid, Leganés, Spain.ORCID 0000-0001-8572-2712
Matteo SireciDepartamento de Electromagnetismo y Física de la Materia and Instituto Carlos I de Física Teórica y Computacional, Universidad de Granada, Granada, Spain.
Miguel A MuñozDepartamento de Electromagnetismo y Física de la Materia and Instituto Carlos I de Física Teórica y Computacional, Universidad de Granada, Granada, Spain.ORCID 0000-0003-0152-9080

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ecological and evolutionary dynamics have been historically regarded as unfolding at broadly separated timescales. However, these two types of processes are nowadays well-documented to intersperse much more tightly than traditionally assumed, especially in communities of microorganisms. Advancing the development of mathematical and computational approaches to shed novel light onto eco-evolutionary problems is a challenge of utmost relevance. With this motivation in mind, here we scrutinize recent experimental results showing evidence of rapid evolution of tolerance by lag in bacterial populations that are periodically exposed to antibiotic stress in laboratory conditions. In particular, the distribution of single-cell lag times-i.e., the times that individual bacteria from the community remain in a dormant state to cope with stress-evolves its average value to approximately fit the antibiotic-exposure time. Moreover, the distribution develops right-skewed heavy tails, revealing the presence of individuals with anomalously large lag times. Here, we develop a parsimonious individual-based model mimicking the actual demographic processes of the experimental setup. Individuals are characterized by a single phenotypic trait: their intrinsic lag time, which is transmitted with variation to the progeny. The model-in a version in which the amplitude of phenotypic variations grows with the parent's lag time-is able to reproduce quite well the key empirical observations. Furthermore, we develop a general mathematical framework allowing us to describe with good accuracy the properties of the stochastic model by means of a macroscopic equation, which generalizes the Crow-Kimura equation in population genetics. Even if the model does not account for all the biological mechanisms (e.g., genetic changes) in a detailed way-i.e., it is a phenomenological one-it sheds light onto the eco-evolutionary dynamics of the problem and can be helpful to design strategies to hinder the emergence of tolerance in bacterial communities. From a broader perspective, this work represents a benchmark for the mathematical framework designed to tackle much more general eco-evolutionary problems, thus paving the road to further research avenues.

Indexed as

Anti-Bacterial AgentsBacterial Physiological PhenomenaDrug Resistance, BacterialAdaptation, PhysiologicalBacteriaBiological EvolutionComputational BiologyComputer SimulationDrug ToleranceMicrobiotaModels, BiologicalPhenotypeStress, PhysiologicalAnti-Bacterial Agents

Identifiers

PMID34555011
PMCPMC8492070

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Registered trials

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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.