The Arabidopsis outward K ⁺ channel GORK mediates flg22-induced K ⁺ efflux and stomatal closure

Transient K ⁺ efflux occurs rapidly following pathogen-associated molecular pattern (PAMP) perception by pattern recognition receptors (PRRs) as part of pattern-triggered immunity (PTI). However, the molecular identities of the K ⁺ channels responsible for PTI-associated K ⁺ efflux and the mechanisms linking immune signaling to K ⁺ channel regulation remain largely unknown. Here, we show that the channel GUARD CELL OUTWARD RECTIFYING K ⁺ (GORK) is required for K ⁺ efflux and stomatal closure induced by flg22, a model PAMP derived from bacterial flagellin. BOTRYTIS-INDUCED KINASE 1 (BIK1), a receptor-like cytoplasmic kinase associated with immune receptor complexes that functions as a central regulator of PTI, interacts with GORK and phosphorylates the channel on the conserved T199 residue in vitro. Electrophysiological analyses indicate that BIK1 inhibits GORK activity in a kinase-dependent manner and that T199 plays an essential role for GORK function. Together, this study identifies GORK as the key K ⁺ channel executing rapid PTI-associated K ⁺ efflux and associated stomatal closure, thus shedding light on the mechanisms of early immune signaling.