CAJ | 학술논문

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。
이잠두（Vicia faba L．）협편하표피위재료，결합기공개도분석화보위세포내원일양화담（NO）수평적측정，연구료 NO 화린지선기순3-격매（PI3K）적최화산물린지선기순3-린산（PI3P）재자외선 B（UV-B）유도기공관폐중적관계。결과현시：UV-B 복사유도잠두보위세포 NO 산생화기공관폐적효응능피 PI3K 억제제옥만청매소（WM）화 LY294002（LY）현저억제。동시，외원 NO석방제초보납（SNP）처리능완전역전 WM 화 LY 대 UV-B 유도기공관폐적억제효응，이 WM 화LY 각불능억제외원 SNP 유도잠두기공관폐적효응。결과설명，재 UV-B 유도잠두기공관폐적신호전도도경중 PI3P 적작용재 NO 상유。
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 phos-phatidylinositol 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 PI3K inhibitors wortmannin (WM)and LY294002 (LY).Meanwhile,exogenous NO-relea-sing 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 PI3P acts upstream of NO in the signal transduction pathway of UV-B-induced stomatal closure of broad bean.