Two phosphatidylinositol 3-kinase components are involved in interactions between Nicotiana benthamiana and Phytophthora by regulating pathogen effectors and host cell death.

Abstract

Phosphatidylinositol 3-phosphate (PtdIns(3)P) has been reported to regulate different physiological processes in plants. PtdIns(3)P is synthesised by the phosphatidylinositol 3-kinase (PI3K) complex which includes common subunits of vacuolar protein sorting (VPS)15, VPS30 and VPS34. Here, we characterised the roles of the important genes NbVPS15, -30 and -34 encoding PI3K components during interactions between Nicotiana benthamiana and Phytophthora pathogens. NbVPS15 and NbVPS34 were upregulated during infection, and plants deficient in these two genes displayed higher resistance to two different Phytophthora pathogens. Silencing NbVPS15 and NbVPS34 decreased the content of PtdIns(3)P in plant cells and the stability of three RxLR (containing the characteristic amino-terminal motif of arginine-X-leucine-arginine, X is any amino acid) effectors. Furthermore, NbVPS15, -30 and -34 were essential for autolysosome formation during Phytophthora capsici infection and limiting programmed cell death (PCD) induced by effectors and elicitors. Taken together, these findings suggest that NbVPS15 and NbVPS34 play a critical role in the resistance of N. benthamiana to Phytophthora pathogens by regulating PtdIns(3)P contents and host PCD.