Evidence map›Paper›PMID 28524864›Full record

ArticleNature communications2017

Mistranslation can enhance fitness through purging of deleterious mutations.

Sinisa Bratulic, Macarena Toll-Riera, Andreas Wagner

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

  1. RNAViruses · 2026
    Review
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  7. Beta-Lactam Antibiotic Resistance Genes in the Microbiome of the Public Transport System of Quito, Ecuador.International journal of environmental research and public health · 2023
    Article
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  14. The impact of mistranslation on phenotypic variability and fitness.Evolution; international journal of organic evolution · 2021
    Article
  15. Review
  16. Article
  17. Article
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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 at 2 institutions in 2 countries.

Sinisa BratulicDepartment of Evolutionary Biology and Environmental Studies, University of Zurich, Winterthurerstrasse 190, Zurich CH-8057, Switzerland.
Macarena Toll-RieraDepartment of Evolutionary Biology and Environmental Studies, University of Zurich, Winterthurerstrasse 190, Zurich CH-8057, Switzerland.
Andreas WagnerDepartment of Evolutionary Biology and Environmental Studies, University of Zurich, Winterthurerstrasse 190, Zurich CH-8057, Switzerland.
University of Zurich · CHSanta Fe Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenotypic mutations are amino acid changes caused by mistranslation. How phenotypic mutations affect the adaptive evolution of new protein functions is unknown. Here we evolve the antibiotic resistance protein TEM-1 towards resistance on the antibiotic cefotaxime in an Escherichia coli strain with a high mistranslation rate. TEM-1 populations evolved in such strains endow host cells with a general growth advantage, not only on cefotaxime but also on several other antibiotics that ancestral TEM-1 had been unable to deactivate. High-throughput sequencing of TEM-1 populations shows that this advantage is associated with a lower incidence of weakly deleterious genotypic mutations. Our observations show that mistranslation is not just a source of noise that delays adaptive evolution. It could even facilitate adaptive evolution by exacerbating the effects of deleterious mutations and leading to their more efficient purging. The ubiquity of mistranslation and its effects render mistranslation an important factor in adaptive protein evolution.

Indexed as

Gene DeletionGenetic FitnessMutationAnti-Bacterial Agentsbeta-LactamasesDrug Resistance, BacterialEscherichia coliEvolution, MolecularGene LibraryGenotypeModels, GeneticMutagenesisPhenotypePolymorphism, Single NucleotideProtein BiosynthesisSelection, GeneticAnti-Bacterial Agentsbeta-Lactamasesbeta-lactamase TEM-1

Identifiers

PMID28524864
PMCPMC5454534
OpenAlexW2614323966

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.