磷脂酶C参与ParA1诱导的烟草悬浮细胞死亡和防卫反应

【目的】研究寄生疫霉Phytophthora parasitica分泌的蛋白激发子ParA1诱导烟草悬浮细胞后,磷脂酶C(phospholipase C,PLC)参与ParA1诱导烟草过敏细胞死亡(hypersensitive cell death,HCD)和防卫反应。【方法】采用药理学方法,在烟草悬浮细胞中添加PLC抑制剂,比较烟草悬浮细胞受ParA1诱导后细胞死亡和多种防卫反应的差别。【结果】PLC特异性抑制剂U73122能完全抑制ParA1引起的烟草悬浮细胞死亡,氧迸发、胞外基质碱化和植保素scopoletin(7-羟基-6-甲氧基香豆素)积累都能显著地被抑制,5种防卫基因hin1、hsr203J、PR(pathogenesis-related)-1a、PR-1b和PAL等的转录表达也都受到U73122不同程度的抑制。【结论】ParA1处理烟草悬浮细胞后,PLC参与了ParA1诱导细胞死亡和防卫反应的信号传导过程。

Involvement of Phospholipase C in Induction of Cell Death and Defense Responses in ParA1-Elicited Tobacco Suspension Cells

【Objective】 Phospholipase C (PLC) was investigated in response to ParA1, a protein elicitor from Phytophthora parasitica, and could trigger cell death and defense responses in tobacco suspension cells. 【Method】 Using a pharmacological approach, tobacco suspension cells pretreated with PLC inhibitors (neomycin and U73122) in ParA1-induced cells were used to compare cell death and a series of defense responses. 【Result】 Tobacco suspension cells treated with ParA1 resulted in defense responses, such as hypersensitive cell death, an oxidative burst, alkalization of the extracellular medium, expression of 5 defense-related genes and accumulation of scopoletin, defense-related genes hin1, hsr203J, PR-1a, PR-1b and PAL were expressed in ParA1-induced cells. Cell death induced by ParA1 was entirely inhibited by the addition of U73122, a PLC specific inhibitor. Oxidative burst, alkalization of the extracellular medium, expression of 5 defense-related genes and scopoletin accumulation was significantly suppressed by U73122, respectively. 【Conclusion】 PLC is required for ParA1-mediated cell death and defense response in tobacco suspension cells which may involve in signal transduction.