Evidence map›Paper›PMID 32687537›Full record

ArticlePLoS pathogens2020

Cross-feeding modulates the rate and mechanism of antibiotic resistance evolution in a model microbial community of Escherichia coli and Salmonella enterica.

Elizabeth M Adamowicz, Michaela Muza, Jeremy M Chacón, William R Harcombe

Abstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed.

  1. Review
  2. Metabolism-Based Biomarkers for Rapid Phenotypic Antibiotic Susceptibility Testing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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  18. An ecological and stochastic perspective on persisters resuscitation.Computational and structural biotechnology journal · 2025
    Article
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  20. Article
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

4 authors.

Elizabeth M AdamowiczDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, Minnesota, United States of America.
Michaela MuzaDepartment of Ecology, Evolution and Behavior, University of Minnesota, St. Paul, Minnesota, United States of America.
Jeremy M ChacónDepartment of Ecology, Evolution and Behavior, University of Minnesota, St. Paul, Minnesota, United States of America.
William R HarcombeDepartment of Ecology, Evolution and Behavior, University of Minnesota, St. Paul, Minnesota, United States of America.ORCID 0000-0001-8445-2052

Funding

Systems biology and the evolutionary dynamics in a synthetic microbial communityR01GM121498 · NIGMS · UNIVERSITY OF MINNESOTA · PI HARCOMBE, WILLIAM · 2017 to 2021
$1.5M
NIGMS NIH HHS R01 GM121498
6 · The paper itself

Abstract

With antibiotic resistance rates on the rise, it is critical to understand how microbial species interactions influence the evolution of resistance. In obligate mutualisms, the survival of any one species (regardless of its intrinsic resistance) is contingent on the resistance of its cross-feeding partners. This sets the community antibiotic sensitivity at that of the 'weakest link' species. In this study, we tested the hypothesis that weakest link dynamics in an obligate cross-feeding relationship would limit the extent and mechanisms of antibiotic resistance evolution. We experimentally evolved an obligate co-culture and monoculture controls along gradients of two different antibiotics. We measured the rate at which each treatment increased antibiotic resistance, and sequenced terminal populations to question whether mutations differed between mono- and co-cultures. In both rifampicin and ampicillin treatments, we observed that resistance evolved more slowly in obligate co-cultures of E. coli and S. enterica than in monocultures. While we observed similar mechanisms of resistance arising under rifampicin selection, under ampicillin selection different resistance mechanisms arose in co-cultures and monocultures. In particular, mutations in an essential cell division protein, ftsI, arose in S. enterica only in co-culture. A simple mathematical model demonstrated that reliance on a partner is sufficient to slow the rate of adaptation, and can change the distribution of adaptive mutations that are acquired. Our results demonstrate that cooperative metabolic interactions can be an important modulator of resistance evolution in microbial communities.

Indexed as

Adaptation, PhysiologicalAmpicillinAnti-Bacterial AgentsBacterial ProteinsCoculture TechniquesDrug Resistance, MicrobialEscherichia coliMicrobial InteractionsModels, TheoreticalMutationRifampinSalmonella entericaAmpicillinAnti-Bacterial AgentsBacterial ProteinsRifampin

Identifiers

PMID32687537
PMCPMC7392344

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LicenceCC BY
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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.