Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity.
Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity.
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DOI：
10.1038/ncomms13099
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发表时间：
2016-10-11
影响因子：
16.6
通讯作者：
Dong, Xinnian
中科院分区：
文献类型：
--
作者：
Liu, Lijing;Sonbol, Fathi-Mohamed;Huot, Bethany;Gu, Yangnan;Withers, John;Mwimba, Musoki;Yao, Jian;He, Sheng Yang;Dong, Xinnian
这是一个明显的难题，植物如何进化效应触发免疫（ETI），涉及程序性细胞死亡（PCD），作为一个主要的防御机制，对生物营养型病原体，因为ETI相关的PCD可能会让他们容易受到坏死的病原体，在死亡的宿主细胞上茁壮成长。有趣的是，在ETI，通常拮抗防御激素，水杨酸（SA）和茉莉酸（JA）分别与防御生物营养型和坏死营养型，都积累到高水平。在这项研究中，我们做出了令人惊讶的发现，JA是RPS2介导的ETI的正调控因子。SA积累后JA应答基因的早期诱导和JA从头合成通过SA受体NPR 3和NPR 4而不是JA受体COI 1激活。我们提供的证据表明，NPR3和NPR4可能介导的JA转录抑制因子JAZs的降解促进这种效果。SA和JA之间的这种独特的相互作用提供了一个可能的解释，植物如何能够抵御活体营养型病原体，而不容易受到坏死型病原体。 水杨酸（SA）和茉莉酸（JA）在植物防御中常起拮抗作用。在这里，Liu等人表明，在针对假单胞菌的效应子触发免疫（ETI）期间，JA信号传导经由涉及SA受体NPR 3和NPR 4的非经典途径被激活，以正向调节ETI。
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.
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