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Wounding-Induced Stomatal Closure Requires Jasmonate-Mediated Activation of GORK K<sup>+</sup> Channels by a Ca<sup>2+</sup> Sensor-Kinase CBL1-CIPK5 Complex.
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 <sup>+</sup> 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 Ca <sup>2+</sup> sensor-kinase complexes. GORK activation strictly depends on plasma membrane targeting and Ca <sup>2+</sup> 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 Ca <sup>2+</sup> signaling in response to biotic stress converges with the ABA-mediated drought stress pathway to facilitate GORK-mediated stomatal closure upon wounding.
abscisic acid, arabidopsis, calcium, guard cell, jasmonic acid, kinase, patch-clamp, phosphorylation, potassium channel, wounding
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