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通过提高摇床转速对烟草细胞施加机械刺激(MS)可诱导其胞内一氧化氮(NO)的快速产生和一氧化氮合酶(NOS)活性的提高,这种MS诱导的NO产生可被NO清除剂cPTIO和NOS抑制剂L-NMMA显著抑制。此外,Ca2+螯合剂EGTA、质膜Ca2+通道阻断剂La3+、胞内Ca2+通道拮抗剂钌红,以及钙调素抑制剂CPZ和TFP预处理均不同程度地抑制了机械刺激诱导的烟草细胞NO的产生,而机械刺激过程中钙调素活性显著上升并与NOS活性和NO含量的变化相一致。这些结果暗示着(类)NOS酶催化的精氨酸依赖途径可能是机械刺激诱发烟草细胞NO产生的主要途径,Ca2+/CaM可能通过调节(类)NOS活性来调控NO的产生。
The mechanical stimulation (MS) on tobacco cells by increasing the speed of shaking can induce the rapid production of intracellular nitric oxide (NO) and the increase of nitric oxide synthase (NOS) activity. Such MS-induced NO production can be NO scavenger cPTIO and NOS inhibitor L-NMMA significantly inhibited. In addition, Ca2 + chelator EGTA, plasma membrane Ca2 + channel blocker La3 +, intracellular Ca2 + channel antagonist ruthenium red, and calmodulin inhibitors CPZ and TFP pretreatment to varying degrees inhibited the mechanical stimulation-induced NO in tobacco cells , Whereas calmodulin activity increased significantly during mechanical stimulation and was consistent with changes in NOS activity and NO content. These results suggest that NOS-catalyzed arginine-dependent pathway may be the main pathway for mechanical stimulation of NO production in tobacco cells. Ca2 + / CaM may regulate NO production by regulating NOS activity.