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.
Nat Commun. 2016 Oct 11;7:13099. doi: 10.1038/ncomms13099.
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.
这是一个明显的难题，植物如何进化出效应子触发的免疫（ETI），涉及程序性细胞死亡（PCD），作为对抗生物病原体的主要防御机制，因为 ETI 相关的 PCD 可能使它们容易受到在死宿主细胞上繁殖的坏死病原体的侵害。有趣的是，在 ETI 期间，通常拮抗的防御激素水杨酸（SA）和茉莉酸（JA）分别与防御生物和坏死病原体有关，两者都积累到高水平。在这项研究中，我们令人惊讶地发现 JA 是 RPS2 介导的 ETI 的正调节剂。SA 积累后 JA 反应基因的早期诱导和从头 JA 合成是通过 SA 受体 NPR3 和 NPR4 激活的，而不是通过 JA 受体 COI1。我们提供的证据表明，NPR3 和 NPR4 可能通过促进 JA 转录阻遏物 JAZs 的降解来介导这种效应。SA 和 JA 之间的这种独特相互作用提供了一种可能的解释，说明植物如何在不使自己易受坏死病原体侵害的情况下对抗生物病原体。
