Involvement of nitric oxide (NO) in signal transduction of stomatal opening

Abstract

The stomatal aperture responses to a range of stimuli including light, humidity, CO2 level, air pollutants and growth regulators (eg. abscisic acid and auxin). Blue light is known to induce stomatal opening through the activation of H+-ATPase. Recent papers have suggested that hydrogen peroxide (H2O2) is involved in abscisic acid-induced stomatal closing. Complex pathways of signal transduction have been considered to regulate these stomatal movements. However, a full picture of the pathways has not been drawn yet. We have recently reported that nitrate reductase produces nitric oxide (NO) by the reduction of nitrite, implicating the enzyme as an NO signal emitter. Here we demonstrate that NO is involved in the mechanism for stomatal opening. We measured stomatal apertures of abaxial epidermis peels of Vicia faba leaves. After the treatment of peels with a NO donor S-nitroso-N-acethylpenisilamine (SNAP), stomatal apertures increased to 1.3-fold of those without SNAP in 15 min. Stomatal aperture was also increased by the presence of supplemental nitrite that can be converted to NO via the reaction of endogenous nitrate reductase. Viagra ©, which inhibits cGMP degradation in the NO signaling pathway of humans, suppressed the H2O2-induced stomatal closing movement. These results suggest that the signal transduction system of guard cells includes an NO-dependent signaling pathway