Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor-like kinase inhibitor BKI1
文献类型： 外文期刊
作者： Lan, Xia 2 ; Liu, Yunxiao 1 ; Song, Shiren 2 ; Yin, Ling 3 ; Xiang, Jiang 2 ; Qu, Junjie 3 ; Lu, Jiang 2 ;
作者机构： 1.China Agr Univ, Coll Food Sci & Nutr Engn, Beijing, Peoples R China
2.Shanghai Jiao Tong Univ, Sch Agr & Biol, Ctr Viticulture & Enol, Shanghai, Peoples R China
3.Guangxi Acad Agr Sci, Guangxi Crop Genet Improvement & Biotechnol Lab, Nanning, Peoples R China
关键词： BKI1; brassinosteroid; downy mildew; ERECTA; Plasmopara viticola; RXLR effector
期刊名称：MOLECULAR PLANT PATHOLOGY （ 影响因子：5.663； 五年影响因子：5.626 ）
ISSN： 1464-6722
年卷期： 2019 年 20 卷 6 期
页码：
收录情况： SCI
摘要： The grapevine downy mildew pathogen Plasmopara viticola secretes a set of RXLR effectors (PvRXLRs) to overcome host immunity and facilitate infection, but how these effectors function is unclear. Here, the biological function of PvRXLR131 was investigated via heterologous expression. Constitutive expression of PvRXLR131 in Colletotrichum gloeosporioides significantly enhanced its pathogenicity on grapevine leaves. Constitutive expression of PvRXLR131 in Arabidopsis promoted Pseudomonas syringae DC3000 and P. syringae DC3000 (hrcC(-)) growth as well as suppressed defence-related callose deposition. Transient expression of PvRXLR131 in Nicotiana benthamiana leaves could also suppress different elicitor-triggered cell death and inhibit plant resistance to Phytophthora capsici. Further analysis revealed that PvRXLR131 interacted with host Vitis vinifera BRI1 kinase inhibitor 1 (VvBKI1), and its homologues in N. benthamiana (NbBKI1) and Arabidopsis (AtBKI1). Moreover, bimolecular fluorescence complementation analysis revealed that PvRXLR131 interacted with VvBKI1 in the plasma membrane. Deletion assays showed that the C-terminus of PvRXLR131 was responsible for the interaction and mutation assays showed that phosphorylation of a conserved tyrosine residue in BKI1s disrupted the interaction. BKI1 was a receptor inhibitor of growth- and defence-related brassinosteroid (BR) and ERECTA (ER) signalling. When silencing of NbBKI1 in N. benthamiana, the virulence function of PvRXLR131 was eliminated, demonstrating that the effector activity is mediated by BKI1. Moreover, PvRXLR131-transgenic plants displayed BKI1-overexpression dwarf phenotypes and suppressed BR and ER signalling. These physiological and genetic data clearly demonstrate that BKI1 is a virulence target of PvRXLR131. We propose that P. viticola secretes PvRXLR131 to target BKI1 as a strategy for promoting infection.
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