A Plasmopara viticola RXLR effector targets a chloroplast protein PsbP to inhibit ROS production in grapevine.

SUMMARY: 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 Vitispiasezkii 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 1O2 signaling pathway in grapevine. RXLR31154 could stabilize PsbP. Together, our data revealed that RXLR31154 reduces H2O2 accumulation and activates the 1O2 signaling pathway through stabilizing PsbP, thereby promoting disease. [ABSTRACT FROM AUTHOR]