Article,

Wounding-Induced Stomatal Closure Requires Jasmonate-Mediated Activation of GORK K(+) Channels by a Ca(2+) Sensor-Kinase CBL1-CIPK5 Complex

, , , , , , , , , , , , , and .
Dev Cell, 48 (1): 87-99 e6 (2019)Forster, Sabrina Schmidt, Lena K Kopic, Eva Anschutz, Uta Huang, Shouguang Schlucking, Kathrin Koster, Philipp Waadt, Rainer Larrieu, Antoine Batistic, Oliver Rodriguez, Pedro L Grill, Erwin Kudla, Jorg Becker, Dirk eng Research Support, Non-U.S. Gov't 2018/12/12 Dev Cell. 2019 Jan 7;48(1):87-99.e6. doi: 10.1016/j.devcel.2018.11.014. Epub 2018 Dec 6..
DOI: 10.1016/j.devcel.2018.11.014

Abstract

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 Ca(2+) sensor-kinase complexes. GORK activation strictly depends on plasma membrane targeting and Ca(2+) 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(2+) signaling in response to biotic stress converges with the ABA-mediated drought stress pathway to facilitate GORK-mediated stomatal closure upon wounding.

Tags

Users

  • @jvsi_all

Comments and Reviews