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 and John Reader ()
Additional contact information
Shaileja Chopra: The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA
Andrés Palencia: European Molecular Biology Laboratory, Grenoble Outstation and Unit of Virus Host-Cell Interactions, UJF-EMBL-CNRS
Cornelia Virus: The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA
Sarah Schulwitz: The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA
Brenda R. Temple: R.L. Juliano Structural Bioinformatics Core Facility, The University of North Carolina at Chapel Hill
Stephen Cusack: European Molecular Biology Laboratory, Grenoble Outstation and Unit of Virus Host-Cell Interactions, UJF-EMBL-CNRS
John Reader: The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: 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.

Date: 2016
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/ncomms12928 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12928

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms12928

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().