Control of Guard Cell Ion Channels by Hydrogen Peroxide and Abscisic Acid Indicates Their Action through Alternate Signaling Pathways

Recent evidence has implicated the action of reactive oxygen species (ROS), notably hydrogen peroxide (H2O2), in abscisic acid (ABA) signaling of guard cells. ABA is known to evoke increases in cytosolic-free Ca2+ (Ca2+i), dependent on flux through Ca2+ channels in the plasma membrane and release from intracellular Ca2+ stores (Grabov and Blatt, 1998; Hamilton et al., 2000; Pei et al., 2000), which inactivates inward-rectifying K+ channels (IK,in) and activates anion channels to bias the plasma membrane for solute efflux and stomatal closure (MacRobbie, 1997; Blatt, 2000;Schroeder et al., 2001). ABA also activates outward-rectifying K+ channels (IK,out) through a parallel rise in cytosolic pH (see Blatt, 2000, and refs. therein). H2O2 was suggested as an intermediate early in ABA signal transduction because when added externally it, too, triggers stomatal closure and is known to activate Ca2+ channels and elevate Ca2+i in many plant cells (Price et al., 1994; Pei et al., 2000; Murata et al., 2001; Schroeder et al., 2001; Zhang et al., 2001b). ROS production is augmented by exogenous ABA and its block by diphenylene iodonium and the abi1 mutant (dominant-negative) protein phosphatase suppresses stomatal closure in Arabidopsis (Pei et al., 2000;Murata et al., 2001; Zhang et al., 2001b).