한빛사논문
Ye-Eun Seo1,2,†, Hye-Young Lee1, Haeun Kim1,2, Xin Yan1,2, Sang A Park1,2, Myung-Shin Kim1,2, Cécile Segonzac1,2, Doil Choi1,2,*, and Hyunggon Mang1,3,†,*
1 Plant Immunity Research Center, Seoul National University, Seoul, 08826, Republic of Korea
2 Department of Agriculture, Forestry and Bioresources, Plant Genomics and Breeding Institute, Seoul National University, Seoul, 08826,
Republic of Korea
3 Department of Southern Area Crop Science, National Institute of Crop Science (NICS), RDA, Miryang, Republic of Korea
† These authors contributed equally to this work.
* Correspondence: Doil Choi, Hyunggon Mang
Abstract
Pathogen effectors can suppress various plant immune responses, suggesting that they have multiple targets in the host. To understand the mechanisms underlying plasma membrane-associated and effector-mediated immunity, we performed Phytophthora capsici RxLR cell death Inducer Suppressing Immune System (CRISIS) screening. In Nicotiana benthamiana, the cell death induced by the RxLR effector CRISIS2 is inhibited by the irreversible plasma membrane H +-ATPase (PMA) activator fusicoccin. Biochemical and gene silencing analyses revealed that CRISIS2 physically and functionally associates with PMAs and induces host cell death independent of immune receptors. CRISIS2 induces apoplastic alkalization by suppressing PMA activity via its association with the C-terminal regulatory domain of PMA. In planta expression of CRISIS2 significantly enhanced the virulence of P. capsici, whereas host-induced gene silencing of CRISIS2 compromised disease symptom and biomass of P. capsici. Our study identified a novel RxLR effector playing multiple roles in the suppression of plant defense and induction of cell death to support the pathogen hemibiotrophic life cycle in the host plant.
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