Abstract
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.