The relationship between NO and H2O2 during UV-B-regulated stomatal movement.

 

The role and the interrelationship of hydrogen peroxide and nitric oxide in the UV-B-induced stomatal closure in broad bean

by He J., Xu H., She X.-P., Song X.-G., Zhao W.-M. (2005)

in Funct. Plant Biol. 32, 237–247. doi: 10.1071/FP04185 –

CrossRef Full Text | Google Scholar

http://www.publish.csiro.au/?paper=FP04185

Abstract

Previous studies have showed that UV-B can stimulate closure as well as opening of stomata. However, the mechanism of this complex effect of UV-B is not clear.

The purpose of this paper is to investigate the role and the interrelationship of H₂O₂ and NO in UV-B-induced stomatal closure in broad bean (Vicia fabaL.).

By epidermal strip bioassay and laser-scanning confocal microscopy, we observed that UV-B-induced stomatal closure could be largely prevented not only by NO scavenger c-PTIO or NO synthase (NOS) inhibitor l-NAME, but also by ascorbic acid (ASC, an important reducing substrate for H₂O₂ removal) or catalase (CAT, the H₂O₂ scavenger), and that UV-B-induced NO and H₂O₂ production in guard cells preceded UV-B-induced stomatal closure.

These results indicate that UV-B radiation induces stomatal closure by promoting NO and H₂O₂ production. In addition, c-PTIO, l-NAME, ASC and CAT treatments could effectively inhibit not only UV-B-induced NO production, but also UV-B-induced H₂O₂ production. Exogenous H₂O₂-induced NO production and stomatal closure were partly abolished by c-PTIO and l-NAME.

Similarly, exogenous NO donor sodium nitroprusside-induced H₂O₂ production and stomatal closure were also partly reversed by ASC and CAT.

These results show a causal and interdependent relationship between NO and H₂O₂ during UV-B-regulated stomatal movement. Furthermore, the l-NAME data also indicate that the NO in guard cells of Vicia faba is probably produced by a NOS-like enzyme.