Evidence map›Paper›PMID 27713402›Full record

ArticleNature communications2016

Structural characterization of antibiotic self-immunity tRNA synthetase in plant tumour biocontrol agent.

Shaileja Chopra, Andrés Palencia, Cornelia Virus, Sarah Schulwitz, Brenda R Temple, Stephen Cusack, John Reader

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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  6. Bacterial translation machinery for deliberate mistranslation of the genetic code.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

7 authors at 2 institutions in 2 countries.

Shaileja ChopraDepartment of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA.
Andrés PalenciaEuropean Molecular Biology Laboratory, Grenoble Outstation and Unit of Virus Host-Cell Interactions, UJF-EMBL-CNRS, UMI 3265, 71, Avenue des Martyrs, CS 90181, 38042 Grenoble Cedex 96 rue Jules Horowitz, BP181, Grenoble Cedex 9 38042, France.
Cornelia VirusDepartment of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA.
Sarah SchulwitzDepartment of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA.
Brenda R TempleR.L. Juliano Structural Bioinformatics Core Facility, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
Stephen CusackEuropean Molecular Biology Laboratory, Grenoble Outstation and Unit of Virus Host-Cell Interactions, UJF-EMBL-CNRS, UMI 3265, 71, Avenue des Martyrs, CS 90181, 38042 Grenoble Cedex 96 rue Jules Horowitz, BP181, Grenoble Cedex 9 38042, France.
John ReaderDepartment of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA.
University of North Carolina at Chapel Hill · USEuropean Molecular Biology Laboratory · FR

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
NCI NIH HHS P30 CA016086
6 · The paper itself

Abstract

Antibiotic-producing microbes evolved self-resistance mechanisms to avoid suicide. The biocontrol Agrobacterium radiobacter K84 secretes the Trojan Horse antibiotic agrocin 84 that is selectively transported into the plant pathogen A. tumefaciens and processed into the toxin TM84. We previously showed that TM84 employs a unique tRNA-dependent mechanism to inhibit leucyl-tRNA synthetase (LeuRS), while the TM84-producer prevents self-poisoning by expressing a resistant LeuRS AgnB2. We now identify a mechanism by which the antibiotic-producing microbe resists its own toxin. Using a combination of structural, biochemical and biophysical approaches, we show that AgnB2 evolved structural changes so as to resist the antibiotic by eliminating the tRNA-dependence of TM84 binding. Mutagenesis of key resistance determinants results in mutants adopting an antibiotic-sensitive phenotype. This study illuminates the evolution of resistance in self-immunity genes and provides mechanistic insights into a fascinating tRNA-dependent antibiotic with applications for the development of anti-infectives and the prevention of biocontrol emasculation.

Indexed as

Evolution, MolecularAgrobacterium tumefaciensDrug Resistance, BacterialGenes, BacterialKineticsLeucine-tRNA LigasePest Control, BiologicalPlant TumorsRNA, TransferLeucine-tRNA LigaseRNA, Transfer

Identifiers

PMID27713402
PMCPMC5059758
OpenAlexW2529296848

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.