Evidence map›Paper›PMID 36062982›Full record

ArticleMolecular biology and evolution2022

Evolutionary History and Strength of Selection Determine the Rate of Antibiotic Resistance Adaptation.

Sandra Cisneros-Mayoral, Lucía Graña-Miraglia, Deyanira Pérez-Morales, Rafael Peña-Miller, Ayari Fuentes-Hernández

Open access · goldAbstract read
In one paragraph

Article in Molecular biology and evolution, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.4field-weighted citation impact, top 4% of its field
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

19 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Genome and transcriptomic analysis of the adaptation ofComputational and structural biotechnology journal · 2024
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  16. Eco-evolutionary dynamics of experimentalMicrobiology (Reading, England) · 2023
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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

5 authors at 2 institutions in 2 countries.

Sandra Cisneros-MayoralPrograma de Biología Sintética, Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, 62210 Cuernavaca, Mexico.
Lucía Graña-MiragliaDepartment of Cell & Systems Biology, University of Toronto, Toronto, Ontario, Canada.
Deyanira Pérez-MoralesPrograma de Biología de Sistemas, Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, 62210 Cuernavaca, Mexico.
Rafael Peña-MillerPrograma de Biología de Sistemas, Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, 62210 Cuernavaca, Mexico.
Ayari Fuentes-HernándezPrograma de Biología Sintética, Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, 62210 Cuernavaca, Mexico.
Universidad Nacional Autónoma de México · MXUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial adaptation to stressful environments often produces evolutionary constraints whereby increases in resistance are associated with reduced fitness in a different environment. The exploitation of this resistance-cost trade-off has been proposed as the basis of rational antimicrobial treatment strategies designed to limit the evolution of drug resistance in bacterial pathogens. Recent theoretical, laboratory, and clinical studies have shown that fluctuating selection can maintain drug efficacy and even restore drug susceptibility, but can also increase the rate of adaptation and promote cross-resistance to other antibiotics. In this paper, we combine mathematical modeling, experimental evolution, and whole-genome sequencing to follow evolutionary trajectories towards β-lactam resistance under fluctuating selective conditions. Our experimental model system consists of eight populations of Escherichia coli K12 evolving in parallel to a serial dilution protocol designed to dynamically control the strength of selection for resistance. We implemented adaptive ramps with mild and strong selection, resulting in evolved populations with similar levels of resistance, but with different evolutionary dynamics and diverging genotypic profiles. We found that mutations that emerged under strong selection are unstable in the absence of selection, in contrast to resistance mutations previously selected in the mild selection regime that were stably maintained in drug-free environments and positively selected for when antibiotics were reintroduced. Altogether, our population dynamics model and the phenotypic and genomic analysis of the evolved populations show that the rate of resistance adaptation is contingent upon the strength of selection, but also on evolutionary constraints imposed by prior drug exposures.

Indexed as

Drug Resistance, BacterialEscherichia coliAdaptation, PhysiologicalAnti-Bacterial AgentsMutationAnti-Bacterial Agentsantibiotic resistancebacterial genomicsexperimental evolutionmathematical modeling

Identifiers

PMID36062982
PMCPMC9512152
OpenAlexW4294666607

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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.