Gene editing of the transmembrane kinase SOAK1 fine-tunes reactive oxygen species production for enhanced disease resistance in potato.

The reactive oxygen species (ROS) burst is a hallmark of immune responses, and its fine-tuned regulation is essential for balancing plant immunity and growth. Although mechanistic understanding of ROS production has improved in Arabidopsis, corresponding knowledge remains sparse in crops, particularly in the non-Brassicaceae species that lack PBL13-mediated negative regulation of the ROS burst. Here, we report an RLCK-V subfamily member in potato, StSOAK1, which negatively regulates disease resistance to the oomycete Phytophthora infestans and the fungus Botrytis cinerea. Furthermore, the potato stsoak1 mutants displayed elevated ROS production upon pathogen infection and immune activation. StSOAK1 interacts with and directly phosphorylates the ROS-producing enzyme StRBOHB at Ser849. Notably, the StSOAK1-StRBOHB complex exhibits dynamic changes upon immune activation. Moreover, the phosphorylation status of the S849 site is essential for StRBOHB protein stability and the function of StRBOHB in regulating ROS burst. Together, our study reveals a regulatory mechanism of potato StRBOHB, which occurs in parallel with its paradigmatic AtPBL13-mediated regulation in Arabidopsis.