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Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity

Author

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  • Lijing Liu

    (Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University)

  • Fathi-Mohamed Sonbol

    (Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University
    Faculty of Dentistry, Sinai University)

  • Bethany Huot

    (and Cell and Molecular Biology Program, Michigan State University)

  • Yangnan Gu

    (Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University)

  • John Withers

    (Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University)

  • Musoki Mwimba

    (Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University)

  • Jian Yao

    (Howard Hughes Medical Institute, Michigan State University
    Western Michigan University)

  • Sheng Yang He

    (Howard Hughes Medical Institute, Michigan State University)

  • Xinnian Dong

    (Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Duke University)

Abstract

It is an apparent conundrum how plants evolved effector-triggered immunity (ETI), involving programmed cell death (PCD), as a major defence mechanism against biotrophic pathogens, because ETI-associated PCD could leave them vulnerable to necrotrophic pathogens that thrive on dead host cells. Interestingly, during ETI, the normally antagonistic defence hormones, salicylic acid (SA) and jasmonic acid (JA) associated with defence against biotrophs and necrotrophs respectively, both accumulate to high levels. In this study, we made the surprising finding that JA is a positive regulator of RPS2-mediated ETI. Early induction of JA-responsive genes and de novo JA synthesis following SA accumulation is activated through the SA receptors NPR3 and NPR4, instead of the JA receptor COI1. We provide evidence that NPR3 and NPR4 may mediate this effect by promoting degradation of the JA transcriptional repressor JAZs. This unique interplay between SA and JA offers a possible explanation of how plants can mount defence against a biotrophic pathogen without becoming vulnerable to necrotrophic pathogens.

Suggested Citation

  • Lijing Liu & Fathi-Mohamed Sonbol & Bethany Huot & Yangnan Gu & John Withers & Musoki Mwimba & Jian Yao & Sheng Yang He & Xinnian Dong, 2016. "Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity," Nature Communications, Nature, vol. 7(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13099
    DOI: 10.1038/ncomms13099
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    Cited by:

    1. Hehong Zhang & Fengmin Wang & Weiqi Song & Zihang Yang & Lulu Li & Qiang Ma & Xiaoxiang Tan & Zhongyan Wei & Yanjun Li & Junmin Li & Fei Yan & Jianping Chen & Zongtao Sun, 2023. "Different viral effectors suppress hormone-mediated antiviral immunity of rice coordinated by OsNPR1," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    2. Jinping Zou & Xinlin Chen & Chenxu Liu & Mingyue Guo & Mukesh Kumar Kanwar & Zhenyu Qi & Ping Yang & Guanghui Wang & Yan Bao & Diane C. Bassham & Jingquan Yu & Jie Zhou, 2023. "Autophagy promotes jasmonate-mediated defense against nematodes," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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