Calcium-dependent ABA signaling functions in stomatal immunity by regulating rapid SA responses in guard cells

Stomatal immunity is mediated by ABA, an osmotic stress-responsive phytohormone that closes stomata via calcium-dependent and-independent signaling pathways. However, the functional involvement of ABA signal transducers in stomatal immunity remains poorly understood. Here, we demonstrate that stomatal immunity was compromised in mutants of the ABA signaling core. We also found that it is a subset of calcium-dependent protein kinases (CPK4/5/6), but not the calcium-independent kinase OST1, that relay the stomatal immune signaling. Surface-inoculated bacteria caused an endogenous ABA-dependent induction of local SA responses, whilst expression of the ABA biosynthetic genes and the ABA levels were not affected in leaf epidermis. Furthermore, flg22-elicited ROS burst was attenuated by mutations in CPK4 and CPK5, and pathogen-induced SA production in leaf epidermis was compromised in cpk4, cpk5, and cpk6 mutants. Our results suggest that CPKs function in stomatal immunity through fine-tuning apoplastic ROS levels as well as reinforcing the localized SA signal in guard cells. It is also envisioned that ABA mediates stomatal responses to biotic and abiotic stresses via two distinct but partially overlapping signaling modules.

Automated summary

Mutants of the ABA signaling core compromised stomatal immunity, with a subset of calcium-dependent protein kinases (CPK4/5/6) playing a role in stomatal immune signaling. Additionally, CPKs regulate apoplastic ROS levels and reinforce the localized SA signal in guard cells, contributing to stomatal immunity.