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

Author

Listed:
  • 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
    Present address: Institute for Advanced Biosciences, Team Host-Pathogen Interactions and Immunity to Infection, INSERM U1209, CNRS UMR5309, Université Grenoble Alpes, Grenoble Cedex 9 38042, France)

  • 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
    Present address: The Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK)

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.

Suggested Citation

  • Shaileja Chopra & Andrés Palencia & Cornelia Virus & Sarah Schulwitz & Brenda R. Temple & Stephen Cusack & John Reader, 2016. "Structural characterization of antibiotic self-immunity tRNA synthetase in plant tumour biocontrol agent," Nature Communications, Nature, vol. 7(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12928
    DOI: 10.1038/ncomms12928
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    Cited by:

    1. Naba K. Das & Nele M. Hollmann & Jeff Vogt & Spiridon E. Sevdalis & Hasan A. Banna & Manju Ojha & Deepak Koirala, 2023. "Crystal structure of a highly conserved enteroviral 5′ cloverleaf RNA replication element," Nature Communications, Nature, vol. 14(1), pages 1-14, December.

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