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木质植物降解病原体胶孢炭疽菌效应物 LtCre1 靶向葡萄树糖信号蛋白 VvRHIP1 以抑制宿主免疫。

The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity.

机构信息

Beijing Key Laboratory of Environment Friendly Management on Fruits Pests in North China, Institute of Plant Protection, Beijing Academy of Agriculture and Forestry Sciences, Beijing 100097, China.

State Key Laboratory of Protein and Plant Gene Research, School of Advanced Agricultural Sciences and School of Life Sciences, Peking-Tsinghua Center for Life Sciences, Peking University, 100871 Beijing, China.

出版信息

J Exp Bot. 2023 Apr 18;74(8):2768-2785. doi: 10.1093/jxb/erad055.

Abstract

Lasiodiplodia theobromae is a causal agent of Botryosphaeria dieback, which seriously threatens grapevine production worldwide. Plant pathogens secrete diverse effectors to suppress host immune responses and promote the progression of infection, but the mechanisms underlying the manipulation of host immunity by L. theobromae effectors are poorly understood. In this study, we characterized LtCre1, which encodes a L. theobromae effector that suppresses BAX-triggered cell death in Nicotiana benthamiana. RNAi-silencing and overexpression of LtCre1 in L. theobromae showed impaired and increased virulence, respectively, and ectopic expression in N. benthamiana increased susceptibility. These results suggest that LtCre1 is as an essential virulence factor for L. theobromae. Protein-protein interaction studies revealed that LtCre1 interacts with grapevine RGS1-HXK1-interacting protein 1 (VvRHIP1). Ectopic overexpression of VvRHIP1 in N. benthamiana reduced infection, suggesting that VvRHIP1 enhances plant immunity against L. theobromae. LtCre1 was found to disrupt the formation of the VvRHIP1-VvRGS1 complex and to participate in regulating the plant sugar-signaling pathway. Thus, our results suggest that L. theobromae LtCre1 targets the grapevine VvRHIP1 protein to manipulate the sugar-signaling pathway by disrupting the association of the VvRHIP1-VvRGS1 complex.

摘要

胶孢炭疽菌是引起葡萄枝枯病的病原菌,该病害严重威胁着全球的葡萄产业。植物病原菌会分泌多种效应子来抑制宿主的免疫反应,从而促进感染的进展,但胶孢炭疽菌效应子操纵宿主免疫的机制还知之甚少。在本研究中,我们对编码胶孢炭疽菌效应子 LtCre1 的基因进行了研究,该效应子能够抑制拟南芥中 BAX 诱导的细胞死亡。RNAi 沉默和 LtCre1 在胶孢炭疽菌中的过表达分别导致了菌株毒力的减弱和增强,而过表达 LtCre1 会导致拟南芥更容易受到感染。这些结果表明 LtCre1 是胶孢炭疽菌的一个重要毒力因子。蛋白-蛋白相互作用研究表明,LtCre1 与葡萄 RGS1-HXK1 互作蛋白 1(VvRHIP1)相互作用。在拟南芥中异位过表达 VvRHIP1 会降低感染程度,这表明 VvRHIP1 增强了植物对胶孢炭疽菌的免疫反应。研究发现 LtCre1 会破坏 VvRHIP1-VvRGS1 复合物的形成,并参与调控植物的糖信号通路。因此,我们的研究结果表明,胶孢炭疽菌 LtCre1 通过破坏 VvRHIP1-VvRGS1 复合物的形成,靶向葡萄 VvRHIP1 蛋白来操纵糖信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ccfb/10112684/a943cec4ca73/erad055f0001.jpg

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