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Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity
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Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity
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Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity
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Journal Article
Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity
2016
Overview
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.
Salicylic acid (SA) and jasmonic acid (JA) often act antagonistically in plant defence. Here, Liu
et al
. show that during effector-triggered immunity (ETI) against
Pseudomonas syringae
, JA signalling is activated via a non-canonical pathway involving the SA receptors, NPR3 and NPR4, to positively regulate ETI.
