Plasmopara viticola Effector PvRXLR10 Targets a Host Phospholipase VvipPLA-IIδ2 to Suppress Plant Immunity in Grapevine

文献类型： 外文期刊

第一作者： Qu, Junjie

作者： Qu, Junjie;Liu, Lulu;Zheng, Chengxu;Guo, Zexi;Sun, Dayun;Pan, Fengying;Yin, Ling;Lu, Jiang

作者机构：

关键词： effector; grapevine; immunity; jasmonic acid; Plasmopara viticola

期刊名称：MOLECULAR PLANT PATHOLOGY （ 影响因子：4.9； 五年影响因子：5.6 ）

ISSN： 1464-6722

年卷期： 2025 年 26 卷 5 期

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收录情况： SCI

摘要： Plasmopara viticola that causes grapevine downy mildew disease in viticulture regions is among the 10 most relevant pathogens worldwide. It secretes a large arsenal of effectors to facilitate colonisation by perturbing host immunity. However, the underlying mechanisms by which P. viticola effectors disturb grapevine defence are still largely unknown. In this study, we report that PvRXLR10, an RXLR effector with a WY domain, promotes P. viticola infection in grapevine and Phytophthora parasitica colonisation in Nicotiana benthamiana. PvRXLR10 interacts with a host patatin-like protein VvipPLA-II delta 2 with phospholipase A2 activity. The WY domain of PvRXLR10 is not responsible for cell death suppression in N. benthamiana but is necessary for PvRXLR10 interaction with VvipPLA-II delta 2. Overexpression and RNAi-mediated suppression of VvipPLA-II delta 2 expression in Vitis vinifera consistently showed that this protein positively regulates plant immunity in response to P. viticola infection. Interestingly, we found that VvipPLA-II delta 2 partially associates with PvRXLR10 at the endoplasmic reticulum (ER). Reverse transcription-quantitative PCR (RT-qPCR) analysis showed that the expression of VvipPLA-II delta 2 was suppressed by PvRXLR10 during P. viticola infection. The overexpression of VvipPLA-II delta 2 in V. vinifera induced higher expression of genes related to jasmonic acid (JA) biosynthesis, signalling pathways and defence response. The evidence indicates the important roles of VvipPLA-II delta 2 in grapevine immunity and P. viticola effector PvRXLR10 targets this protein to promote its infection.

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