Evidence map›Paper›PMID 33235191›Full record

ArticleNature communications2020

High-throughput laboratory evolution reveals evolutionary constraints in Escherichia coli.

Tomoya Maeda, Junichiro Iwasawa, Hazuki Kotani, Natsue Sakata, Masako Kawada, Takaaki Horinouchi, Aki Sakai, Kumi Tanabe, Chikara Furusawa

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 93 citations in OpenAlex.

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  8. Advances in adaptive laboratory evolution applications forSynthetic and systems biotechnology · 2025
    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

9 authors at 2 institutions in 1 country.

Tomoya MaedaRIKEN Center for Biosystems Dynamics Research, 6-2-3 Furuedai, Suita, Osaka, 565-0874, Japan. tomoya.maeda@riken.jp.ORCID 0000-0002-2024-7794
Junichiro IwasawaDepartment of Physics, The University of Tokyo, 7-3-1 Hongo, Tokyo, 113-0033, Japan.ORCID 0000-0002-2560-5650
Hazuki KotaniRIKEN Center for Biosystems Dynamics Research, 6-2-3 Furuedai, Suita, Osaka, 565-0874, Japan.
Natsue SakataRIKEN Center for Biosystems Dynamics Research, 6-2-3 Furuedai, Suita, Osaka, 565-0874, Japan.
Masako KawadaRIKEN Center for Biosystems Dynamics Research, 6-2-3 Furuedai, Suita, Osaka, 565-0874, Japan.
Takaaki HorinouchiRIKEN Center for Biosystems Dynamics Research, 6-2-3 Furuedai, Suita, Osaka, 565-0874, Japan.
Aki SakaiRIKEN Center for Biosystems Dynamics Research, 6-2-3 Furuedai, Suita, Osaka, 565-0874, Japan.
Kumi TanabeRIKEN Center for Biosystems Dynamics Research, 6-2-3 Furuedai, Suita, Osaka, 565-0874, Japan.
Chikara FurusawaRIKEN Center for Biosystems Dynamics Research, 6-2-3 Furuedai, Suita, Osaka, 565-0874, Japan. chikara.furusawa@riken.jp.ORCID 0000-0003-3554-4975
RIKEN Center for Biosystems Dynamics Research · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the constraints that shape the evolution of antibiotic resistance is critical for predicting and controlling drug resistance. Despite its importance, however, a systematic investigation of evolutionary constraints is lacking. Here, we perform a high-throughput laboratory evolution of Escherichia coli under the addition of 95 antibacterial chemicals and quantified the transcriptome, resistance, and genomic profiles for the evolved strains. Utilizing machine learning techniques, we analyze the phenotype-genotype data and identified low dimensional phenotypic states among the evolved strains. Further analysis reveals the underlying biological processes responsible for these distinct states, leading to the identification of trade-off relationships associated with drug resistance. We also report a decelerated evolution of β-lactam resistance, a phenomenon experienced by certain strains under various stresses resulting in higher acquired resistance to β-lactams compared to strains directly selected by β-lactams. These findings bridge the genotypic, gene expression, and drug resistance gap, while contributing to a better understanding of evolutionary constraints for antibiotic resistance.

Indexed as

Escherichia coliEvolution, MolecularAnti-Bacterial Agentsbeta-Lactam ResistanceDrug Resistance, Multiple, BacterialGenes, BacterialGenotypeMicrobial Sensitivity TestsAnti-Bacterial Agents

Identifiers

PMID33235191
PMCPMC7686311
OpenAlexW3108628125

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.