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

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.

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Citation

Published Version (Please cite this version)

10.1038/ncomms13099

Publication Info

Liu, Lijing, Fathi-Mohamed Sonbol, Bethany Huot, Yangnan Gu, John Withers, Musoki Mwimba, Jian Yao, Sheng Yang He, et al. (2016). Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity. Nature communications, 7(1). p. 13099. 10.1038/ncomms13099 Retrieved from https://hdl.handle.net/10161/21721.

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Scholars@Duke

He

Sheng-Yang He

Benjamin E. Powell Distinguished Professor of Biology

Interested in the fascinating world of plants, microbes or inter-organismal communication and co-evolution? Please contact Prof. Sheng-Yang He (shengyang.he@duke.edu; hes@msu.edu).

Millions of years of co-evolution between plants and microbes have resulted in an intricate web of attack, counter-attack, decoy, and hijacking mechanisms in biology. Moreover, co-evolution between plants and microbes is greatly impacted by ongoing climate change. In our lab, we probe “host-microbe-climate” interactions to answer the following fundamental questions: (1) How do microbial pathogens infect a susceptible host? (2) How do plants select beneficial microbiomes to ensure health? (3) How do climate conditions impact disease and immunity?      

We use contemporary methods to address these questions, including those commonly used in molecular genetics, genomics, biochemistry, cell biology, bioinformatics, microbiology, plant biology, co-evolution and infectious disease biology.    

Dong

Xinnian Dong

Arts and Sciences Distinguished Professor of Biology

Using Arabidopsis thaliana as a model system, my laboratory studies the mechanisms of plant defense against microbial pathogens. We focus on a specific response known as systemic acquired resistance (SAR). SAR, which can be induced by a local infection, provides the plants with long lasting, systemic resistance against a broad spectrum of pathogens. Salicylic acid (SA; an active ingredient of aspirin) has been found to be the endogenous signal of SAR. Using a genetic approach, our laboratory identified genes involved in the regulation of SAR. Molecular and genetic analyses are being carried out to understand the gene function and to elucidate the SAR signaling pathway. These SAR-regulating genes are also favorite targets for molecular engineering of disease-resistance crops.


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