CPK6 functions as a positive regulator of MeJA signaling in Arabidopsis stomata


The Arabidopsis calcium-dependent protein kinase, CPK6, functions as a positive regulator of methyl jasmonate signaling in guard cells.

Munemasa S., Hossain M. A., Nakamura Y., Mori I. C., Murata Y. (2011)

in Plant Physiol. 155, 553–561. – doi: 10.1104/pp.110.162750 –

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text – [PMC free article] [PubMed] – 


MeJA-induced stomatal closure in Arabidopsis CPK3, CPK6, CPK4, and CPK11 gene disruption mutants. A, MeJA-induced stomatal closure in the wild type (WT) and cpk3-1, cpk6-1, cpk3-1/cpk6-1, cpk4-1, cpk11-2, and cpk4-1/11- 2 mutants. B, MeJA-induced stomatal closure in the cpk6-1 and cpk6-2 mutants. Twenty averages from three independent experiments (60 total stomata per bar) are shown. Error bars represent se. – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075756/bin/PP_162750_gs_f1.jpg


Previous studies have demonstrated that methyl jasmonate (MeJA) induces stomatal closure dependent on change of cytosolic free calcium concentration 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 four Arabidopsis (Arabidopsis thaliana) CDPKs, CPK3, CPK6, CPK4, and CPK11, are involved in abscisic acid signaling in guard cells.

It is also known that there is an interaction between MeJA and abscisic acid signaling in guard cells.

In this study, we examined the 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 the broad expression pattern of CPK6, we did not find other remarkable MeJA-insensitive phenotypes in the cpk6-1 mutant. The whole-cell patch-clamp analysis revealed that MeJA activation of nonselective Ca(2+)-permeable cation channels is impaired in the cpk6-1 mutant.

Consistent with this result, MeJA-induced transient cytosolic free calcium concentration increments were reduced in the cpk6-1 mutant. MeJA failed to activate slow-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 as in the 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.


Published by

Willem Van Cotthem

Honorary Professor of Botany, University of Ghent (Belgium). Scientific Consultant for Desertification and Sustainable Development.

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