Abstract
Phytohormone abscisic acid (ABA) inhibits blue light-dependent stomatal opening and enhances the stomatal closure under drought stress by unknown mechanisms. Here we show that nitric oxide (NO), a second messenger of ABA signaling, specifically inhibits blue light-dependent stomatal opening. Blue light-dependent stomatal opening and H+ pumping were inhibited by a NO donor SNP. All of these inhibitions were restored by c-PTIO, a specific NO scavenger. Importantly, c-PTIO partially blocked the inhibitions of blue light-dependent stomatal opening and H+ pumping by ABA. Furthermore, SNP inhibited blue light-dependent phosphorylation of the plasma membrane H+-ATPase and a subsequent binding of a 14-3-3 protein. However, SNP had no significant effect on the phosphorylation of phototropins, blue light receptors of stomatal opening. These results suggest that NO is responsible for the inhibition of blue light-dependent stomatal opening by ABA through the intercept of blue light signaling between phototropins and the H+-ATPase.