PSKR: An LRR-RLK, Enhances Oxidative Stress Tolerance by Modulating ROS-Driven Stomatal Closure

Stomatal closure is a key adaptive response that plants employ to mitigate oxidative stress, a process tightly regulated by hydrogen peroxide (H₂O₂) signaling in guard cells. Despite its importance, the molecular mechanisms controlling H₂O₂ homeostasis during stomatal regulation remain poorly understood. In this study, we identify the leucine-rich repeat receptor-like kinase (LRR-RLK) Phytosulfokine Receptor (PSKR) as a positive regulator of stomatal closure under oxidative stress. Overexpression of AtPSKR1 and OsPSKR10 in Arabidopsis conferred enhanced oxidative stress tolerance, evidenced by reduced malondialdehyde (MDA) and ROS accumulation, elevated proline levels, and increased activities of antioxidant enzymes relative to wild-type (WT) and mutant plants. RT-qPCR analyses further revealed significant higher expression of multiple stress-responsive genes in PSKR overexpressing transgenic lines under stress. Our findings suggest that PSKR may contribute to H₂O₂-mediated stomatal closure through enhanced OST1 expression and interaction with plasma membrane aquaporins (PIPs). Mechanistically, PSKR promotes H₂O₂-mediated stomatal closure by upregulating OST1 expression and directly interacting with plasma membrane aquaporins (PIPs). Membrane-based split-ubiquitin assays (MbSUS) and Bimolecular Fluorescence Complementation assay (BiFC) confirmed a physical interaction between PSKR and PIP proteins, with conserved Asn and Lys residues essential for binding. Together, these findings uncover a previously uncharacterized PSKR-mediated regulatory module that integrates ROS signaling with stomatal movement, thereby enhancing abiotic stress tolerance in plants.