期刊
MOLECULAR PLANT
卷 11, 期 8, 页码 1067-1083出版社
CELL PRESS
DOI: 10.1016/j.molp.2018.05.009
关键词
RXLR effector; Avr3a; FKBP; ER stress; immunity; Phytophthora capsici
资金
- China Agriculture Research System [CARS-09]
- National Natural Science Foundation of China [31125022, 31561143007]
- Program of Introducing Talents of Innovative Discipline to Universities (Project 111) from the State Administration of Foreign Experts Affairs [B18042]
Phytophthora pathogens secrete a large arsenal of effectors that manipulate host processes to create an environment conducive to pathogen colonization. However, the underlying mechanisms by which Phytophthora effectors manipulate host plant cells still remain largely unclear. In this study, we report that PcAvr3a12, a Phytophthora capsici RXLR effector and a member of the Avr3a effector family, suppresses plant immunity by targeting and inhibiting host plant peptidyl-prolyl cis-trans isomerase (PPlase). Overexpression of PcAvr3a12 in Arabidopsis thaliana enhanced plant susceptibility to P. capsici. FKBP15-2, an endoplasmic reticulum (ER)-localized protein, was identified as a host target of PcAvr3a12 during early P. capsici infection. Analyses of A. thaliana T-DNA insertion mutant (fkbp15-2), RNAi, and overexpression lines consistently showed that FKBP15-2 positively regulates plant immunity in response to Phytophthora infection. FKBP15-2 possesses PPlase activity essential for its contribution to immunity but is directly suppressed by PcAvr3a12. Interestingly, we found that FKBP15-2 is involved in ER stress sensing and is required for ER stress-mediated plant immunity. Taken together, these results suggest that P. capsici deploys an RXLR effector, PcAvr3a12, to facilitate infection by targeting and suppressing a novel ER-localized PPlase, FKBP15-2, which is required for ER stress-mediated plant immunity.
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