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 H
2O
2 accumulation and activated the
1O
2 signaling pathway in grapevine. RXLR31154 could stabilize PsbP. Together, our data revealed that RXLR31154 reduces H
2O
2 accumulation and activates the
1O
2 signaling pathway through stabilizing PsbP, thereby promoting disease.
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