The cascade mechanisms of nitric oxide as a second messenger of ultraviolet B in inhibiting mesocotyl elongations.

In this report, a number of physiological aspects was examined during developmental growth of maize seedling's mesocotyl. It was found that ultraviolet B (UVB) radiation was able to significantly induce nitric oxide synthase (NOS) activities and speedup the release of apparent nitric oxide (NO) of mesocotyl and that exogenous NO donor's rhizospheric treatments may mimic the responses of the mesocotyl to UVB radiation, such as the inhibition of mesocotyl elongation, the decrease in exo- and endoglucanase activities and the increase in protein content of cell wall of mesocotyl. When the seedlings were treated with N-nitro-L-arginine, an inhibitor of NOS, the mesocotyl elongation was promoted, the exo- and endoglucanase activities were raised and the protein content was reduced. However, under UVB radiation, the effects of exogenous NO on several physiological aspects of mesocotyl were similar to those of exogenous reactive oxygen species (ROS) eliminator, N-acetyl-cysteine. All the physiological changes were associated with either the exogenous NO supply or the activities of NOS in plant. Accordingly, it is assumed that reduction in mesocotyl length caused by UVB radiation was possibly achieved through modification of the chemical properties of the cell wall polysaccharides, which was induced by NO and ROS synergically mediated changes in exo- and endo-beta-D-glucanases activities in cell walls, and NO was one of the main signaling molecule of UVB radiation in inhibiting mesocotyl elongations. So NO might function as both a second messenger and an antioxidant of UVB radiation during developmental growth of the mesocotyl.