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GhCPK33 negatively regulates defense against Verticillium dahliae by phosphorylating GhOPR3

Update Time: 2018-09-03 09:31:12Click: times
Qin Hu, Longfu Zhu, Xiangnan zhang, Qianqian Guan, Shenghua Xiao, Ling Min, Xianlong Zhang.2018.Plant Physiology


Verticillium wilt, caused by the soil-borne fungus Verticillium dahliae, is a destructive vascular disease in plants. Approximately 200 dicotyledonous plant species in temperate and subtropical regions are susceptible to this notorious pathogen. Previous studies showed that jasmonic acid (JA) plays a crucial role in plant-V. dahliae interactions. V. dahliae infection generally induces significant JA accumulation in local and distal tissues of the plant. Although JA biosynthesis and the associated enzymes have been intensively studied, the precise mechanism regulating JA biosynthesis upon V. dahliae infection remains unknown. Here, we identified calcium-dependent protein kinase GhCPK33 from upland cotton (Gossypium hirsutum) as a negative regulator of resistance to V. dahliae that directly manipulates JA biosynthesis. Knock-down of GhCPK33 by Agrobacterium-mediated virus-induced gene silencing constitutively activated JA biosynthesis and JA mediated-defense responses, and enhanced resistance to V. dahliae. Further analysis revealed that GhCPK33 interacts with 12-oxophytodienoate reductase 3 (GhOPR3) in peroxisomes. GhCPK33 phosphorylates GhOPR3 at Thr246, leading to decreased stability of GhOPR3, which consequently limits JA biosynthesis. We propose that GhCPK33 is a potential molecular target for improving resistance to Verticillium wilt disease in cotton.