Interaction of intracellular hydrogen peroxide accumulation with nitric oxide production in abscisic acid signaling in guard cells

Abstract

Reactive oxygen species and nitric oxide (NO center dot) concomitantly play essential roles in guard cell signaling. Studies using catalase mutants have revealed that the inducible and constitutive elevations of intracellular hydrogen peroxide (H2O2) have different roles: only the inducible H2O2 production transduces the abscisic acid (ABA) signal leading stomatal closure. However, the involvement of inducible or constitutive NO center dot productions, if exists, in this process remains unknown. We studied H2O2 and NO center dot mobilization in guard cells of catalase mutants. Constitutive H2O2 level was higher in the mutants than that in wild type, but constitutive NO center dot level was not different among lines. Induced NO center dot and H2O2 levels elicited by ABA showed a high correlation with each other in all lines. Furthermore, NO center dot levels increased by exogenous H2O2 also showed a high correlation with stomatal aperture size. Our results demonstrate that ABA-induced intracellular H2O2 accumulation triggers NO center dot production leading stomatal closure.