A Plasmopara viticola RXLR effector targets a chloroplast protein PsbP to inhibit ROS production in grapevine
A Plasmopara viticola RXLR effector targets a chloroplast protein PsbP to inhibit ROS production in grapevine
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DOI：
10.1111/tpj.15252
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发表时间：
2021-04-24
期刊：
影响因子：
7.2
通讯作者：
Xu, Yan
中科院分区：
文献类型：
--
作者：
Liu, Ruiqi;Chen, Tingting;Xu, Yan
病原体分泌大量的效应物，操纵寄主过程，创造有利于病原体定植的环境。然而，霜霉病菌效应器操纵寄主植物细胞的潜在机制仍然很大程度上不清楚。在本研究中，我们报道了一种葡萄疫霉RXLR效应蛋白RXLR31154在葡萄疫霉感染的早期阶段高表达。在本研究中，RXLR31154在葡萄(Vitis Vinifera)和本氏烟草(Nictiana Benthamiana)中的稳定表达分别促进了葡萄疫霉和辣椒疫霉菌对叶片的定殖。通过酵母双杂交筛选，确定PSBP基因编码的23 kDa放氧增强子2(VpOEE2或VpPsbP)为RXLR31154的寄主靶标。VpPsbP在葡萄中的过表达增强了对葡萄黄萎病的敏感性，而在本底拟青霉中的PSBP同源物NbPsbPs的沉默降低了辣椒疫霉的定殖率，表明PSBP是一种敏感因子。RXLR31154和VpPsbP蛋白共定位于叶绿体中。此外，VpPsbP减少了葡萄体内H_2O_2的积累，并激活了O-1(2)信号通路。RXLR31154可稳定PSBP。综上所述，我们的数据揭示了RXLR31154通过稳定PSBP来减少过氧化氢的积累并激活O-1(2)信号通路，从而促进疾病的发生。
Pathogens secrete a large number of effectors that manipulate host processes to create an environment conducive to pathogen colonization. However, the underlying mechanisms by which Plasmopara viticola effectors manipulate host plant cells remain largely unclear. In this study, we reported that RXLR31154, a P. viticola RXLR effector, was highly expressed during the early stages of P. viticola infection. In our study, stable expression of RXLR31154 in grapevine (Vitis vinifera) and Nicotiana benthamiana promoted leaf colonization by P. viticola and Phytophthora capsici, respectively. By yeast two-hybrid screening, the 23-kDa oxygen-evolving enhancer 2 (VpOEE2 or VpPsbP), encoded by the PsbP gene, in Vitis piasezkii accession Liuba-8 was identified as a host target of RXLR31154. Overexpression of VpPsbP enhanced susceptibility to P. viticola in grapevine and P. capsici in N. benthamiana, and silencing of NbPsbPs, the homologs of PsbP in N. benthamiana, reduced P. capcisi colonization, indicating that PsbP is a susceptibility factor. RXLR31154 and VpPsbP protein were co-localized in the chloroplast. Moreover, VpPsbP reduced H2O2 accumulation and activated the O-1(2) signaling pathway in grapevine. RXLR31154 could stabilize PsbP. Together, our data revealed that RXLR31154 reduces H2O2 accumulation and activates the O-1(2) signaling pathway through stabilizing PsbP, thereby promoting disease.