NLR surveillance of pathogen interference with hormone receptors induces immunity
NLR surveillance of pathogen interference with hormone receptors induces immunity
复制标题
NLR 监测病原体干扰激素受体诱导免疫力
DOI：
10.1038/s41586-022-05529-9
复制
发表时间：
2022-12-14
期刊：
影响因子：
64.8
通讯作者：
Tao, Xiaorong
中科院分区：
文献类型：
--
作者：
Chen, Jing;Zhao, Yanxiao;Tao, Xiaorong
植物激素信号通路在细胞表面模式识别受体和细胞内核苷酸结合的富含亮氨酸重复序列的免疫受体(NLR)介导的病原体防御中起着重要作用。病原体已经进化出反防御策略，以操纵植物激素信号通路，以抑制免疫力和提高毒力(3)。然而，关于植物先天免疫系统对病原菌干扰植物激素信号的监测知之甚少。辣椒(Capsicum Chinense)NLR TSW识别番茄斑点枯萎病毒(TSWV)编码的非结构蛋白NSS，含有一个异常大的富含亮氨酸重复序列(LRR)结构域。结构建模预测Tsw的LRR结构域与茉莉酸受体COI1、生长素受体TIR1和斯特里内酯受体伙伴Max2的LRR结构域相似。这表明NSS可以直接靶向激素受体信号来促进感染，而TSW已经进化出一种类似于植物激素受体LRR的LRR来诱导免疫。在这里，我们发现NSS与COI1、TIR1和MAX2通过一个共同的抑制因子--TCP21--直接与这些植物激素受体相互作用。NSS增强COI1、TIR1或Max2与TCP21的相互作用，并阻止相应转录抑制物的降解，从而使植物激素介导的宿主对病毒的免疫失效。Tsw还与TCP21直接相互作用，这种相互作用被病毒NSS增强。TCP21的下调影响了TSW介导的TSWV防御。综上所述，我们的发现表明，病原体效应器针对TCP21来抑制植物激素受体功能，促进毒力，而植物NLR蛋白已经进化到将这种干扰识别为抗毒力策略，从而激活免疫。
Phytohormone signalling pathways have an important role in defence against pathogens mediated by cell-surface pattern recognition receptors and intracellular nucleotide-binding leucine-rich repeat class immune receptors(1,2) (NLR). Pathogens have evolved counter-defence strategies to manipulate phytohormone signalling pathways to dampen immunity and promote virulence(3). However, little is known about the surveillance of pathogen interference of phytohormone signalling by the plant innate immune system. The pepper (Capsicum chinense) NLR Tsw, which recognizes the effector nonstructural protein NSs encoded by tomato spotted wilt orthotospovirus (TSWV), contains an unusually large leucine-rich repeat (LRR) domain. Structural modelling predicts similarity between the LRR domain of Tsw and those of the jasmonic acid receptor COI1, the auxin receptor TIR1 and the strigolactone receptor partner MAX2. This suggested that NSs could directly target hormone receptor signalling to promote infection, and that Tsw has evolved a LRR resembling those of phytohormone receptors LRR to induce immunity. Here we show that NSs associates with COI1, TIR1 and MAX2 through a common repressor-TCP21-which interacts directly with these phytohormone receptors. NSs enhances the interaction of COI1, TIR1 or MAX2 with TCP21 and blocks the degradation of corresponding transcriptional repressors to disable phytohormone-mediated host immunity to the virus. Tsw also interacts directly with TCP21 and this interaction is enhanced by viral NSs. Downregulation of TCP21 compromised Tsw-mediated defence against TSWV. Together, our findings reveal that a pathogen effector targets TCP21 to inhibit phytohormone receptor function, promoting virulence, and a plant NLR protein has evolved to recognize this interference as a counter-virulence strategy, thereby activating immunity.