NO可能作为Ca^2＋的下游信号介导乙烯诱导的蚕豆气孔关闭

以蚕豆（Vicia faba L．）为材料，利用药理学实验，结合激光共聚焦显微技术和分光光度法．探讨Ca^2＋和一氧化氮（nitric oxide，NO）在乙烯（ethylene，Eth）调控气孔运动信号转导中的作用。结果表明．光下乙烯利（0．004％，0．04％，0．4％）可诱导蚕豆叶片气孔关闭，且具有时间和剂量效应：NO清除剂cPTIO、硝酸还原酶（nitrate reductase，NR）抑制剂NaN3及胞外Ca^2＋螯合剂EGTA可部分逆转乙烯诱导的气孔关闭；乙烯能够明显增加气孔保卫细胞NO水平；提高蚕豆叶片NO含量和NR活性．并且NO的含量变化与NR活性的变化趋势基本一致；NR抑制剂NaN3可抑制乙烯诱导的气孔保卫细胞和叶片NO含量的增加；清除胞外Ca^2＋可减弱乙烯对NO含量和NR活性的诱导效应。说明Ca^2＋和NO均参与乙烯诱导的蚕豆气孔关闭，且NO（主要由NR途径合成）可能位于Ca^2＋下游参与调控这一信号转导过程。

NO MAY FUNCTION IN THE DOWNSTREAM OF Ca2+IN ETHYLENE INDUCED STOMATAL CLOSURE IN Vicia faba L.

Through pharmacological combined with laser scanning confocal microscope （LSCM） and spectrophotography to study the role of Ca^2＋ and NO in signaling during Vicia faba L. stomatal movement response to ethylene （Eth）. The results showed that treatment with ethephon （0.004%, 0.04%, 0.4%） resulted in a time- and dose-dependent stomatal closure under light. NO scavenger cPTIO, nitrate reductase inhibitor NAN3, or extracellular Ca^2＋ chelation EGTA reduced ethylene-induced stomatal closure. Moreover, ethylene was shown to enhance nitric oxide levels and, corresponding, nitrate reductase activity. Inhibition of the nitrate reductase diminished ethylene-induced NO production in both stomatal guard cell and leaf. Finally, ethylene-induced NO levels and nitrate reductase activity decreased when Ca^2＋ was compromised, On the basis of biochemical and pharmacological experimental results, we can conclude that Ca^2＋and NO were involved in the signal transduction pathway of ethylene induced stomatal closure. Nitrate reductase-derived NO may represents a novel downstream component of Ca^2＋signaling cascade during ethylene-induced stomatal movement in Vicia faba L.