Evidence map›Paper›PMID 32031639›Full record

ArticleMolecular biology and evolution2020

Population Bottlenecks Strongly Influence the Evolutionary Trajectory to Fluoroquinolone Resistance in Escherichia coli.

Linnéa Garoff, Franziska Pietsch, Douglas L Huseby, Tua Lilja, Gerrit Brandis, Diarmaid Hughes

Abstract read
In one paragraph

Article in Molecular biology and evolution, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

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  13. Synthetic genomes unveil the effects of synonymous recoding.bioRxiv : the preprint server for biology · 2024
    Article
  14. Mutation bias and adaptation in bacteria.Microbiology (Reading, England) · 2023
    Review
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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

6 authors.

Linnéa GaroffDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Franziska PietschDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Douglas L HusebyDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Tua LiljaDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Gerrit BrandisDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Diarmaid HughesDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental evolution is a powerful tool to study genetic trajectories to antibiotic resistance under selection. A confounding factor is that outcomes may be heavily influenced by the choice of experimental parameters. For practical purposes (minimizing culture volumes), most experimental evolution studies with bacteria use transmission bottleneck sizes of 5 × 106 cfu. We currently have a poor understanding of how the choice of transmission bottleneck size affects the accumulation of deleterious versus high-fitness mutations when resistance requires multiple mutations, and how this relates outcome to clinical resistance. We addressed this using experimental evolution of resistance to ciprofloxacin in Escherichia coli. Populations were passaged with three different transmission bottlenecks, including single cell (to maximize genetic drift) and bottlenecks spanning the reciprocal of the frequency of drug target mutations (108 and 1010). The 1010 bottlenecks selected overwhelmingly mutations in drug target genes, and the resulting genotypes corresponded closely to those found in resistant clinical isolates. In contrast, both the 108 and single-cell bottlenecks selected mutations in three different gene classes: 1) drug targets, 2) efflux pump repressors, and 3) transcription-translation genes, including many mutations with low fitness. Accordingly, bottlenecks smaller than the average nucleotide substitution rate significantly altered the experimental outcome away from genotypes observed in resistant clinical isolates. These data could be applied in designing experimental evolution studies to increase their predictive power and to explore the interplay between different environmental conditions, where transmission bottlenecks might vary, and resulting evolutionary trajectories.

Indexed as

Anti-Bacterial AgentsEvolution, MolecularFluoroquinolonesDrug Resistance, BacterialEscherichia coliGenetic LinkagePhenotypeWhole Genome SequencingAnti-Bacterial AgentsFluoroquinolonesantibiotic resistancebottleneck sizeciprofloxacinEscherichia coliexperimental evolutionmutation supply

Identifiers

PMID32031639
PMCPMC7253196

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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.