Cysteine-rich receptor-like kinases OsCRK19 and OsCRK22 interact with OsRbohI to modulate ROS production and disease resistance in rice.

Reactive oxygen species (ROS) burst is a hallmark response of plant innate immunity. ROS production must be under tight control since inappropriate accumulation is toxic. In rice, OsRbohI is the key NADPH oxidase responsible for ROS generation. However, the upstream kinases regulating OsRbohI activity remain unknown. Here, we identified two cysteine-rich receptor-like kinases, OsCRK19 and OsCRK22, as regulators of OsRbohI. OsCRK19 and OsCRK22 bind to N- both termini of OsRbohI. OsCRK19/22-OsRbohI interactions are constitutive and not responding to PAMP elicitation. OsCRK19 and OsCRK22 phosphorylates OsRbohI, indicating direct regulation. Furthermore, double mutants, rather than single mutants, of Oscrk19 and Oscrk22 exhibit compromised pathogen-associated molecular pattern (PAMP)-triggered ROS burst and increased susceptibility to rice blast fungus Magnaporthe oryzae (M. oryzae), indicating functional redundancy. This study identifies OsCRK19 and OsCRK22 as upstream kinases of OsRbohI, defining a novel regulatory module that regulates PAMP-induced ROS production and disease resistance in rice. The findings refine the regulation of ROS burst in rice immunity and highlight OsCRK-OsRbohI signaling as a target for crop improvement.