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以蚕豆(Vicia faba)表皮条为材料,利用磷脂酰肌醇3-激酶(PI3K)的抑制剂沃曼青霉素(WM)和LY294002(LY)抑制磷脂酰肌醇3-磷酸(PI3P)的形成,并结合气孔开度分析及激光扫描共聚焦显微镜技术,探讨暗诱导蚕豆气孔关闭过程中PI3P与过氧化氢(H2O2)和一氧化氮(NO)之间的相互关系。结果表明,WM和LY显著抑制暗诱导的保卫细胞H2O2和NO的形成以及气孔的关闭,但不能抑制外源H2O2和NO诱导的气孔关闭,外源H2O2和NO处理能完全逆转WM和LY对暗诱导的气孔关闭的抑制效应。实验结果暗示,在暗诱导的气孔关闭的信号转导途径中PI3P在信号分子H2O2和NO的上游起作用。
The epidermal strips of Vicia faba were used to inhibit the formation of phosphatidylinositol 3-phosphate (PI3P) with inhibitors of phosphatidylinositol 3-kinase (PI3K), warfarin (WM) and LY294002 (LY) The relationship between PI3P and hydrogen peroxide (H2O2) and nitric oxide (NO) during dark-induced stomatal closure was investigated by combining stomatal opening analysis and laser scanning confocal microscopy. The results showed that both WM and LY significantly inhibited H2O2 and NO formation and stomatal closure in dark-induced guard cells but not in stomatal closure induced by exogenous H2O2 and NO. Both exogenous H2O2 and NO treatment reversed WM and LY completely Inhibitory effect of stomatal closure induced. Experimental results suggest that PI3P acts upstream of the signaling molecules H2O2 and NO in the dark-induced stomatal closure signal transduction pathway.