in rcn1 mutant (p = 0.87 and 0.25 for MeJA and ABA, respectively) in contrast to wild type. On the other hand, the NO donor, SNP induced stomatal closure both in wild type and rcn1 mutant (data not shown). These results are consistent with our previous results, i.e., NO is involved in both MeJA-and ABA-induced stomatal closure and functions downstream of the branching point of MeJA and ABA signaling in Arabidopsis guard cells. 7 Our finding implies that protein phosphatase 2A might positively regulate NO levels in guard cells (Fig. 2). NO production by nitric oxide synthase (NOS) and nitrate reductase (NR) plays important roles in physiological processes in plants. 3,4 It has been shown that NO functions downstream of ROS production in ABA signaling in guard cells. 5 NO mediates elevation of cytosolic free Ca 2+ concentration ([Ca 2+ ] cyt ), inactivation of inward-rectifying K + channels and activation of S-type anion channels, 6 which are known to be key factors in MeJA-and ABA-induced stomatal closure. 2,[7][8][9] It has been reported that ROS was not induced by MeJA and ABA in the MeJA-and ABA-insensitive mutant, rcn1 in which the regulatory subunit A of protein phosphatase 2A, RCN1, is impaired. 7,10 We examined NO production induced by MeJA and ABA in rcn1 guard cells (Fig. 1). NO production by MeJA and ABA was impaired Significance of differences between data sets was assessed by Student's t-test analysis in this paper. We regarded differences at the level of p < 0.05 as significant.