Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this wo...Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this work, Our experiment showed that NO exists in guard cell of Vicia faba L., and NO is involved in signal transduction of JA- induced stomata closuring: (ⅰ) JA enhances NO synthesis in guard cell; (ⅱ) both JA and NO induced stomatal closure, and had dose response to their effects; (ⅲ) there are synergetic correlation between JA and lower NO concentration in regu- lation of stomatal movement; (ⅳ) JA-induced stomatal closure was largely prevented by 2-phenyl-4,4,5,5-tetrame- thylimidazoline-1-oxyl-3-oxide (PTIO), a specific NO scav- enger. An inhibitor of NO synthase (NOS) in mammalian cells, NG-nitro-L-Arg-methyl eater (L-NAME) also inhibits plant NOS, repressing JA-induced NO generation and JA-induced stomatal closure. We presumed that NO mainly comes from NOS after JA treatment.展开更多
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/...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.展开更多
基金This work was supported by the National Natural Science Foundation of China(Grant No.30370141)Doctor's Fund of College&University Education(Grant No.2002001918)Fund of Education Department of Shandong Province(Grant No.J04C13).
文摘Nitric oxide (NO) and Jasmonic acid (JA) are two key signaling molecules involved in many and diverse biological pathways in plants. Growing evidence suggested that NO signaling interacts with JA signaling. In this work, Our experiment showed that NO exists in guard cell of Vicia faba L., and NO is involved in signal transduction of JA- induced stomata closuring: (ⅰ) JA enhances NO synthesis in guard cell; (ⅱ) both JA and NO induced stomatal closure, and had dose response to their effects; (ⅲ) there are synergetic correlation between JA and lower NO concentration in regu- lation of stomatal movement; (ⅳ) JA-induced stomatal closure was largely prevented by 2-phenyl-4,4,5,5-tetrame- thylimidazoline-1-oxyl-3-oxide (PTIO), a specific NO scav- enger. An inhibitor of NO synthase (NOS) in mammalian cells, NG-nitro-L-Arg-methyl eater (L-NAME) also inhibits plant NOS, repressing JA-induced NO generation and JA-induced stomatal closure. We presumed that NO mainly comes from NOS after JA treatment.
基金the National KeyBasic Research Special Funds of China (Grant No. G1999011700)
文摘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.
