The Kinase OsCPK4 Regulates a Buffering Mechanism That Fine-Tunes Innate Immunity.

Abstract

The calcium-dependent protein kinase OsCPK4 has been demonstrated to play important roles in salt and drought tolerance, plant growth, and development in rice (Oryza sativa). However, little is known about molecular mechanisms underlying OsCPK4 function in rice immunity. In this study, we demonstrated that the generation of oxidative burst and pathogenesis-related gene expression triggered by microbe-associated molecular patterns were significantly enhanced in the oscpk4 mutants. These mutant lines are more resistant to bacterial blight and fungal blast diseases than the wild-type plants, indicating that OsCPK4 negatively regulates innate immunity in rice. OsCPK4 was further identified to interact with a receptor-like cytoplasmic kinase OsRLCK176. OsRLCK176 accumulation is negatively regulated by OsCPK4. Interestingly, the kinase-dead OsCPK4 promotes OsRLCK176 degradation more strongly than the wild-type protein. OsCPK4 and OsRLCK176 mutually phosphorylate each other and form a feedback loop. Moreover, the kinase activity and phosphorylation of OsCPK4 and OsRLCK176 contribute to the stability of OsRLCK176. These findings indicate that the kinase-inactive OsCPK4 promotes OsRLCK176 degradation and restricts plant defenses, whereas the activation of OsCPK4-OsRLCK176 phosphorylation circuit invalidates the OsRLCK176 degradation machinery, thus enhancing plant immunity. Collectively, the study proposes a novel defense buffering mechanism mediated by OsCPK4, which fine-tunes microbe-associated molecular pattern-triggered immunity in rice.