摘要
用外源水杨酸（ｓａｌｉｃｙｌｉｃ ａｃｉｄ，ＳＡ）处理烟草（ Ｎｉｃｏｔｉａｎａｔａｂａｃｕｍ Ｌ．） 培养细胞，证实ＳＡ能诱导脂质过氧化，抑制过氧化氢酶活性并诱导ＰＲ＿１ 基因的表达。对苯二酚和Ｈ２Ｏ２ 也能不同程度地诱导烟草培养细胞的脂质过氧化和ＰＲ＿１ 基因的表达，但不能抑制过氧化氢酶活性。ｍＲＮＡ 和蛋白合成抑制剂（ 鹅膏覃碱和环己亚胺） 不能诱导烟草培养细胞的脂质过氧化和ＰＲ＿１ 基因的表达，但与ＳＡ协同作用能更有效地诱导烟草培养细胞的脂质过氧化，但强烈地抑制ＳＡ诱导的ＰＲ＿１ 基因的表达。因而推测，ＳＡ或其他诱导物可能通过和过氧化氢酶或植物体内其他大分子相互作用产生活性代谢物或自由基，诱导脂质过氧化，进而激活抗性基因的表达。实验结果表明。
Salicylic acid (SA) could inhibit catalase activity, induce rapid lipid peroxidation and PR _1 gene expression of the tobacco (Nicotiana tabacum L.) cell culture which was incubated with exogenous SA. ρ_dihydroxybenzene and H 2O 2 could also induce lipid peroxidation and PR _1 gene expression at different level, but they were not able to inhibit the catalase activity of tobacco cells. Inhibitors of mRNA and protein_synthesis (α_amanitine and cycloheximide, respectively) could not induce both lipid peroxidation and PR _1 gene expression of tobacco cell culture. However, coordinated action with SA respectively, α_amanitine or cycloheximide was able to induce lipid peroxidation effectively, but strongly blocked the activation of PR _1 gene expression by SA in tobacco cell culture. These results suggested that the generation of reactive metabolites or free radicals, which were induced by SA or other inducers through reaction with catalase or other compounds, initiated lipid peroxidation, subsequently activated pathogen_resistance genes expression. Obviously the lipid peroxidation molecule played an important role in SA signal transduction in tobacco.
基金
广东省自然科学基金
中山大学"211"基础性科学研究前沿基金
广州市科学基金
国家自然科学基金
关键词
烟草
水杨酸
脂质过氧化
保护基因
Tobacco, Salicylic acid, Lipid peroxidation, Defense gene
