Involvement of OST1 Protein Kinase and PYR/PYL/RCAR Receptors in Methyl Jasmonate-Induced Stomatal Closure in Arabidopsis Guard Cells

Methyl jasmonate (MeJA) induces stomatal closure. It has been shown that stomata of many ABA-insensitive mutants are also insensitive to MeJA, and a low amount of ABA is a prerequisite for the MeJA response. However, the molecular mechanisms of the interaction between ABA and MeJA signaling remain to be elucidated. Here we studied the interplay of signaling of the two hormones in guard cells using the quadruple ABA receptor mutant pyr1 pyl1 pyl2 pyl4 and ABA-activated protein kinase mutants ost1-2 and srk2e. In the quadruple mutant, MeJA-induced stomatal closure, H2O2 production, nitric oxide (NO) production, cytosolic alkalization and plasma membrane Ca(2+)-permeable current (ICa) activation were not impaired. At the same time, the inactivation of the inward-rectifying K(+) current was impaired. In contrast to the quadruple mutant, MeJA-induced stomatal closure, H2O2 production, NO production and cytosolic alkalization were impaired in ost1-2 and srk2e as well as in aba2-2, the ABA-deficient mutant. The activation of ICa was also impaired in srk2e. Collectively, these results indicated that OST1 was essential for MeJA-induced stomatal closure, while PYR1, PYL1, PYL2 and PYL4 ABA receptors were not sufficient factors. MeJA did not appear to activate OST1 kinase activity. This implies that OST1 mediates MeJA signaling through an undetectable level of activity or a non-enzymatic action. MeJA induced the expression of an ABA synthesis gene, NCED3, and increased ABA contents only modestly. Taken together with previous reports, this study suggests that MeJA signaling in guard cells is primed by ABA and is not brought about through the pathway mediated by PYR1, PYL1 PYL2 and PYL4.

This is an Accepted Manuscript of an article published by Oxford University Press