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以蚕豆为材料,研究一氧化氮合酶(NOS)途径在SO2诱发气孔运动中的作用.研究发现:浓度7.5~200μmol·L-1的SO2衍生物处理后,蚕豆叶面气孔开度减小,气孔开度与SO2衍生物浓度呈负相关;SO2衍生物处理组叶组织中NOS活性增强;加入NO清除剂c-PTIO或NOS抑制剂L-NAME可抑制SO2衍生物诱发的气孔关闭;SO2衍生物处理组保卫细胞内NO和Ca2+水平升高,用c-PTIO降低胞内NO水平后Ca2+水平随之下降.结果表明,SO2衍生物胁迫可诱发保卫细胞内NO合成增加,NO通过调节胞内Ca2+水平升高,激活下游信号转导途径,调节气孔运动;NOS途径介导的NO合成参与了SO2胁迫下蚕豆气孔运动的调节.
The function of nitric oxide synthase (NOS) pathway in stomatal movement induced by SO2was studied using broad bean as a material.The results showed that stomatal opening of Vicia faba reduced after 7.5 ~ 200μmol·L-1 SO2 derivative treatment , And the stomatal opening was negatively correlated with the concentration of SO2 derivatives; the activity of NOS in leaves of SO2 derivatives treatment group was enhanced; and NO-scavenger c-PTIO or NOS inhibitor L-NAME could inhibit the stomatal closure induced by SO2 derivatives; SO2 The levels of NO and Ca2 + in guard cells were increased with the treatment of derivative and the level of Ca2 + decreased with the increase of intracellular NO level with c-PTIO. The results showed that SO2 derivatives could induce the increase of NO synthesis in guard cells, The intracellular Ca2 + level was increased, the downstream signal transduction pathway was activated, and stomatal movement was regulated. NOS pathway-mediated NO synthesis was involved in stomatal movement regulation in Vicia faba under SO2 stress.