A Phytophthora capsici virulence effector associates with NPR1 and suppresses plant immune responses

A Phytophthora capsici virulence effector associates with NPR1 and suppresses plant immune responses
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辣椒疫霉毒力效应子与 NPR1 相关并抑制植物免疫反应

DOI:
10.1186/s42483-019-0013-y
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发表时间:
2019-01-01
影响因子:
3.4
通讯作者:
Zhang, Meixiang
Zhang, Meixiang
中科院分区:
农林科学2区
文献类型:
--
作者:
Li, Qi;Chen, Yanyu;Zhang, Meixiang

文献摘要

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水杨酸(SA)在植物免疫中起着至关重要的调节作用。 NPR1(发病机制相关非表达蛋白 1)是一种 SA 受体,在 SA 信号转导中发挥着关键作用。然而,针对 NPR1 促进感染的病原体效应子却鲜有报道。在这里,我们鉴定了辣椒疫霉效应子 RxLR48,它与 NPR1 相关,促进 P。辣椒感染,是病原体毒力所必需的。此外,我们证明RxLR48促进NPR1的核定位并抑制其蛋白酶体介导的降解,这表明RxLR48通过靶向中央调节因子NPR1来抑制SA信号传导。此外,我们还发现 RxLR48 还可以抑制模式触发免疫(PTI)。总之,我们的研究表明 P.辣椒通过靶向 SA 和 PTI 途径来抑制植物免疫力。
Salicylic acid (SA) plays a crucial regulatory role in plant immunity. NPR1 (non-expressor of pathogenesis related-1) is a SA receptor and plays a pivotal role in SA signaling. However, pathogen effectors which target NPR1 to promote infection have rarely been reported. Here, we identified aPhytophthora capsicieffector RxLR48 that associates with NPR1, facilitatesP. capsiciinfection and is required for pathogen virulence. Furthermore, we demonstrated that RxLR48 promotes NPR1’s nuclear localization and inhibits its proteasome-mediated degradation, suggesting that RxLR48 suppresses SA signaling by targeting the central regulator NPR1. In addition, we showed that RxLR48 also suppresses pattern-triggered immunity (PTI). Together, our research indicates thatP. capsicisuppresses plant immunity by targeting SA and PTI pathways.