NO and Ca2+: Critical Components of Cytosolic Signaling Systems Involved in Stomatal Immune Responses

Abstract Nitric oxide (NO) is a secondary messenger involved in a wide range of signal transduction pathways, including plant immune responses. NO production can be triggered by various microbial pathogens and endogenous defense signaling molecules. Some phyllosphere pathogens invade plant leaves through the leaf surface stomatal pore formed by a pair of guard cells. To prevent the first-line attack, a series of innate immune signaling cascades occur in the guard cells that trigger stomatal closure. NO is one of the critical components involved in stomatal closure, evidenced by using pharmacological reagents and genetic resources. NO biosynthesis in plant cells is thought to occur by two pathways. One is the l -arginine-dependent pathway and the other is the nitrate reduction pathway. However, enzymes responsible for NO synthesis in the l -arginine-dependent pathway are still unidentified. Therefore the currently available NO synthesis related mutants are nia1 , nia2 (the two genes encoding nitrate reductase) and noa1 , an NO-associated gene mistakenly characterized as the NO synthase previously. Studies on stomatal defense signaling have demonstrated an interdependency between NO and several other secondary messengers, such as Ca 2+ , reactive oxygen species and cGMP and the gasotransmitter H 2 S. These findings indicate that NO is downstream from those signaling molecules. However, recent studies have shown a distinct function of NO that NO-derived moieties bind to certain molecules, resulting in S-nitrosylation of cysteine and tyrosine nitration. NO-associated modification has been identified in several molecules involved in guard cell signaling, indicating a feed-forward role that NO could play in the guard cell. Perspectives and insights on how NO contributes to stomatal immunity through its interplay with other signaling molecules using genetic approaches are proposed and discussed.