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Interfering TAL effectors of Xanthomonas oryzae neutralize R-gene-mediated plant disease resistance

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  • Zhiyuan Ji

    (School of Agriculture and Biology/State Key Laboratory of Microbial Metabolism, Shanghai Jiao Tong University
    Development and Cell Biology, Iowa State University)

  • Chonghui Ji

    (Development and Cell Biology, Iowa State University)

  • Bo Liu

    (Development and Cell Biology, Iowa State University)

  • Lifang Zou

    (School of Agriculture and Biology/State Key Laboratory of Microbial Metabolism, Shanghai Jiao Tong University)

  • Gongyou Chen

    (School of Agriculture and Biology/State Key Laboratory of Microbial Metabolism, Shanghai Jiao Tong University)

  • Bing Yang

    (Development and Cell Biology, Iowa State University)

Abstract

Plant pathogenic bacteria of the genus Xanthomonas possess transcription activator-like effectors (TALEs) that activate transcription of disease susceptibility genes in the host, inducing a state of disease. Here we report that some isolates of the rice pathogen Xanthomonas oryzae use truncated versions of TALEs (which we term interfering TALEs, or iTALEs) to overcome disease resistance. In comparison with typical TALEs, iTALEs lack a transcription activation domain but retain nuclear localization motifs and are expressed from genes that were previously considered pseudogenes. We show that the rice gene Xa1, encoding a nucleotide-binding leucine-rich repeat protein, confers resistance against X. oryzae isolates by recognizing multiple TALEs. However, the iTALEs present in many isolates interfere with the otherwise broad-spectrum resistance conferred by Xa1. Our findings illustrate how bacterial effectors that trigger disease resistance in the host can evolve to interfere with the resistance process and, thus, promote disease.

Suggested Citation

  • Zhiyuan Ji & Chonghui Ji & Bo Liu & Lifang Zou & Gongyou Chen & Bing Yang, 2016. "Interfering TAL effectors of Xanthomonas oryzae neutralize R-gene-mediated plant disease resistance," Nature Communications, Nature, vol. 7(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13435
    DOI: 10.1038/ncomms13435
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