磷脂酶D对ParA1诱导的烟草的细胞死亡和过氧化氢及莨菪亭积累的影响  

Effect of Phospholipase D on Induction of Cell Death,Hydrogen Peroxide and Scopoletin Accumulation in Tobacco Cells Treated with ParA1

作　　者：魏芳芳[1] 王蕾[1] 梁元存[1] 王玉军[1] 

机构地区：[1]山东农业大学植物保护学院,山东泰安271018

出　　处：《中国生物化学与分子生物学报》2010年第10期949-954,共6页Chinese Journal of Biochemistry and Molecular Biology

基　　金：山东省教育厅资助项目(No.J08LF06)~~

摘　　要：利用药理学方法,研究了烟草寄生疫霉(Phytophthora parasitica)分泌的蛋白激发子ParA1诱导烟草悬浮细胞后,磷脂酶D对ParA1诱导的过敏细胞死亡和其它防卫反应的影响.用100nmol/LParA1处理烟草悬浮细胞后能够诱导细胞死亡、过氧化氢和莨菪亭的积累.磷脂酶D抑制剂正丁醇能够抑制ParA1诱导的这些防卫反应,仲丁醇所起的抑制作用比正丁醇小,正丁醇和仲丁醇产生的抑制效果具有浓度依赖效应.而叔丁醇不能抑制ParA1诱导的这些反应.结果表明,磷脂酶D参与了ParA1诱导烟草悬浮细胞的信号传导过程.Phospholipase D （PLD） plays an important role in plants,including responses to abiotic and biotic stresses.Effect of PLD signaling in tobacco suspension cells induced by ParA1,a proteinous elicitor from Phytophthora parasitica,was elucidated.Via a pharmacological approach,tobacco suspension cells treated with PLD inhibitors in ParA1-induced cells was used to compare changes in defense responses.Hypersensitive cell death,hydrogen peroxide and scopoletin accumulation induced by ParA1 were strongly inhibited by 1-butanol,a transphosphatidylation substrate,while treatment with 2-butanol had much less effect.Additionally,treatment with 1-butanol and 2-butanol had inhibitory effect in a dose-dependent manner.In contrast,in ParA1-treated cell suspensions,tert-butanol,used as a negative control,had no inhibitory effect.These results suggest that ParA1-mediated pathway needed PLD signaling in tobacco suspension cells.

关 键 词：磷脂酶D ParA1 细胞死亡 过氧化氢 莨菪亭 

分 类 号：S432.2[农业科学—植物病理学]