Title : The Arabidopsis Calcium Dependent Protein Kinase, CPK6, functions as a Positive Regulator of Methyl Jasmonate Signaling in Guard Cells
Previous studies have demonstrated that methyl jasmonate (MeJA) induces stomatal closure dependent on change of cytosolic free calcium concentration ([Ca(2+)](cyt)) in guard cells. However, these molecular mechanisms of intracellular Ca(2+) signal perception remain unknown. Calcium-dependent protein kinases (CDPKs) function as Ca(2+) signal transducers in various plant physiological processes. It has been reported that Arabidopsis four CDPKs, CPK3, CPK6, CPK4, and CPK11 are involved in abscisic acid (ABA) signaling in guard cells. It is also known that there is an interaction between MeJA and ABA signaling in guard cells. In this study, we examined roles of these CDPKs in MeJA signaling in guard cells using Arabidopsis mutants disrupted in the CDPK genes. Disruption of the CPK6 gene impaired MeJA-induced stomatal closure but disruption of the other CDPK genes did not. Despite broad expression pattern of CPK6, we did not find other remarkable MeJA-insensitive phenotype in the cpk6-1 mutant. The whole-cell patch clamp technique showed that MeJA activation of non-selective Ca(2+)-permeable cation (I(Ca)) channels was impaired in the cpk6-1 mutant. Consistent with this result, MeJA-induced transient [Ca(2+)](cyt) increments were reduced in the cpk6-1 mutant. MeJA failed to activate slow-type (S-type) anion channels in the cpk6-1 guard cells. Production of early signal components, reactive oxygen species and nitric oxide, in guard cells was elicited by MeJA in the cpk6-1 mutant like wild type. These results provide genetic evidence that CPK6 has a different role from CPK3 and functions as a positive regulator of MeJA signaling in Arabidopsis guard cells.