The microRNA miR393 re-directs secondary metabolite biosynthesis away from camalexin and towards glucosinolates

Alexandre Robert-Seilaniantz, Dan MacLean, Yusuke Jikumaru, Lionel Hill, Shinjiro Yamaguchi, Yuji Kamiya, Jonathan D.G. Jones

    研究成果: Article査読

    135 被引用数 (Scopus)

    抄録

    Summary flg22 treatment increases levels of miR393, a microRNA that targets auxin receptors. Over-expression of miR393 renders plants more resistant to biotroph pathogens and more susceptible to necrotroph pathogens. In contrast, over-expression of AFB1, an auxin receptor whose mRNA is partially resistant to miR393 degradation, renders the plant more susceptible to biotroph pathogens. Here we investigate the mechanism by which auxin signalling and miR393 influence plant defence. We show that auxin signalling represses SA levels and signalling. We also show that miR393 represses auxin signalling, preventing it from antagonizing SA signalling. In addition, over-expression of miR393 increases glucosinolate levels and decreases the levels of camalexin. Further studies on pathogen interactions in auxin signalling mutants revealed that ARF1 and ARF9 negatively regulate glucosinolate accumulation, and that ARF9 positively regulates camalexin accumulation. We propose that the action of miR393 on auxin signalling triggers two complementary responses. First, it prevents suppression of SA levels by auxin. Second, it stabilizes ARF1 and ARF9 in inactive complexes. As a result, the plant is able to mount a full SA response and to re-direct metabolic flow toward the most effective anti-microbial compounds for biotroph resistance. We propose that miR393 levels can fine-tune plant defences and prioritize resources. The Plant Journal

    本文言語English
    ページ(範囲)218-231
    ページ数14
    ジャーナルPlant Journal
    67
    2
    DOI
    出版ステータスPublished - 2011 7

    ASJC Scopus subject areas

    • 遺伝学
    • 植物科学
    • 細胞生物学

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