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

摘要

The effects and the relationship between sali-cylic acid (SA) and nitric oxide (NO) on Vicia faba L. stomatal movement were studied. The results here showed that exogenous SA and NO induced stomatal closure, 100 mmol/L SA induced a rapid and striking NO increase in the cytosol of guard cells. This phenomenon was largely pre- vented by 200 mmol/L 2-phenyl-4,4,5,5-tetramethylimida- zoline-1-oxyl-3-oxide (PTIO), a specific NO scavenger, and 25 mmol/L NG-nitro-L-Arg-methyl eater (L-NAME), an in- hibitor 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-a]quinoxalin-1-one (ODQ), an inhibitor of guanylate cyclase, and nicotinamide, an antago- nist 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 stomatal closure.