PI3P和NO在UV-B诱导蚕豆气孔关闭中的关系

The interactions of PI3P and NO in UV-B-induced stomatal closure of broad bean

以蚕豆(Vicia faba L.)叶片下表皮为材料,结合气孔开度分析和保卫细胞内源一氧化氮(NO)水平的测定,研究了NO和磷脂酰肌醇3-激酶(PI3K)的催化产物磷脂酰肌醇3-磷酸(PI3P)在紫外线B(UV-B)诱导气孔关闭中的关系。结果显示:UV-B辐射诱导蚕豆保卫细胞NO产生和气孔关闭的效应能被PI3K抑制剂沃曼青霉素(WM)和LY294002(LY)显著抑制。同时,外源NO释放剂硝普钠(SNP)处理能完全逆转WM和LY对UV-B诱导气孔关闭的抑制效应,而WM和LY却不能抑制外源SNP诱导蚕豆气孔关闭的效应。结果说明,在UV-B诱导蚕豆气孔关闭的信号转导途径中PI3P的作用在NO上游。

By stomatal bioassay and measurement of endogenous nitric oxide（NO）level in guard cells,the interactions of NO and phosphatidylinositol 3-phosphate（PI3P）[the product of phosphatidylinositol 3-kinase（PI3K）]in UV-B-induced stomatal closure were studied in the epidermal strips of abaxial surface of broad bean（Vicia faba L.）leaves.The results showed that both the NO production in guard cells and stomatal closure induced by UV-B were significantly inhibited by PI3 Kinhibitors wortmannin（WM）and LY294002（LY）.Meanwhile,exogenous NO-releasing compound sodium nitroprusside（SNP）could completely reverse the inhibitory effect of LY and WM on the UV-B-induced stomatal closure,and WM and LY could not inhibit exogenous SNP-induced stomatal closure of broad bean.These results indicate that PI3 Pacts upstream of NO in the signal transduction pathway of UV-B-induced stomatal closure of broad bean.