Guard cells integrate various hormone signals and environmental cues to balance plant gas exchange and transpiration. The wounding-associated hormone jasmonic acid (JA) and the drought hormone abscisic acid (ABA) both trigger stomatal closure. In contrast to ABA however, the molecular mechanisms of JA-induced stomatal closure have remained largely elusive. Here, we identify a fast signaling pathway for JA targeting the K+ efflux channel GORK. Wounding triggers both local and systemic stomatal closure by activation of the JA signaling cascade followed by GORK phosphorylation and activation through CBL1-CIPK5 Ca2+ sensor-kinase complexes. GORK activation strictly depends on plasma membrane targeting and Ca2+ binding of CBL1-CIPK5 complexes. Accordingly, in gork, cbl1, and cipk5 mutants, JA-induced stomatal closure is specifically abolished. The ABA-coreceptor ABI2 counteracts CBL1-CIPK5-dependent GORK activation. Hence, JA-induced Ca2+ signaling in response to biotic stress converges with the ABA-mediated drought stress pathway to facilitate GORK-mediated stomatal closure upon wounding. •Wounding triggers stomatal closure by activating COI1-dependent guard cell jasmonate signaling•The guard cell K+ efflux channel GORK is required for jasmonate-induced stomatal closure•The Ca2+ sensor-kinase CBL1-CIPK5 complex phosphorylates and activates the GORK channel•Kinase channel activation is antagonized by ABI2, indicating jasmonate and ABA crosstalk Plant stomata regulate gas exchange with the environment in response to various signals, including the wounding-associated hormone jasmonate. Förster et al. delineate the relevant signaling pathway downstream of jasmonate, modulating the activity of the K+ efflux channel GORK, and identify an interaction with abscisic acid (ABA) signaling.