Ethylene mediates UV-B-induced stomatal closure via peroxidase-dependent hydrogen peroxide synthesis in Vicia faba L.

Ultraviolet B (UV-B) radiation is an important environmental signal for plant growth and development, but its signal transduction mechanism is unclear. UV-B is known to induce stomatal closure via hydrogen peroxide (H2O2), and to affect ethylene biosynthesis. As ethylene is also known to induce stomatal closure via H2O2 generation, the possibility of UV-B-induced stomatal closure via ethylene-mediated H2O2 generation was investigated in Vicia faba by epidermal strip bioassay, laser-scanning confocal microscopy, and assays of ethylene production. It was found that H2O2 production in guard cells and subsequent stomatal closure induced by UV-B radiation were inhibited by interfering with ethylene biosynthesis as well as ethylene signalling, suggesting that ethylene is epistatic to UV-B radiation in stomatal movement. Ethylene production preceded H2O2 production upon UV-B radiation, while exogenous ethylene induced H2O2 production in guard cells and subsequent stomatal closure, further supporting the conclusion. Inhibitors for peroxidase but not for NADPH oxidase abolished H2O2 production upon UV-B radiation in guard cells, suggesting that peroxidase is the source of UV-B-induced H2O2 production. Taken together, our results strongly support the idea that ethylene mediates UV-B-induced stomatal closure via peroxidase-dependent H2O2 generation.