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Nat Commun. 2016 Oct 11;7:13099. doi: 10.1038/ncomms13099.

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

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Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Department of Biology, Duke University, Durham, North Carolina 27708, USA.
Department of Basic Sciences, Faculty of Dentistry, Sinai University, Al Arish, North Sinai 45518, Egypt.
Department of Energy Plant Research Laboratory, and Cell and Molecular Biology Program, Michigan State University, East Lansing, Michigan 48824, USA.
Howard Hughes Medical Institute, Department of Energy Plant Research Laboratory, and Department of Plant Biology, Michigan State University, East Lansing, Michigan 48824, USA.
Department of Biological Sciences, Western Michigan University, Kalamazoo, Michigan 49008, USA.


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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