Involvement of nitric oxide in the signal transduction of salicylic acid regulating stomatal movement

The effects and the relationship between salicylic acid (SA) and nitric oxide (NO) on Vicia a a. stomatal movement were studied. The results here showed that exogenous SA and NO induced stomatal closure, 100 mumol/L SA induced a rapid and striking NO increase in the cytosol of guard cells. This phenomenon was largely prevented by 200 tmol/L 2-phenyl-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide (PTIO), a specific NO scavenger, and 25 mumol/L N-G-nitro-L-Arg-methyl eater (L-NAME), an inhibitor of NO synthase (NOS) in mammalian cells that also inhibits plant NOS. In addition, SA-induced stomatal closure was largely prevented by PTIO and L-NAME. These results provide evidence that guard cells generate NO in response to SA via NOS-like activity, and that such NO production is required for full stomatal closure in response to SA. H-(1,2,4)-oxadiazole-[4,3-alquinoxalin-1-one (ODQ), an inhibitor of guanylate cyclase, and nicotinamide, an antagonist of cADPR production, inhibited the effects of SA- and NO-induced stomatal closure. It suggests that both cGMP and cADPR might mediate the signal transduction of SA and NO-induced stomata] closure.