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

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.