Ca2+对水杨酸诱发的丹参幼苗丹酚酸B生物合成的影响

Effects of Ca2+ on salicylic-acid induced biosynthesis of salvianolic acid B in young seedlings of Salvia miltiorrhiza Bunge

摘要:

为研究Ca2+在水杨酸诱导丹参幼苗丹酚酸B生物合成过程中的作用，分别用激光共聚焦显微镜和高效液相色谱仪检测胞外Ca2+通道抑制剂Vp和LaCl3，胞内Ca2+通道抑制剂LiCl以及胞内钙调素拮抗剂TFP处理前、后水杨酸诱导丹参叶片保卫细胞内Ca2+荧光强度和丹酚酸B含量的变化。结果表明，水杨酸 (SA) 处理后6 min即可诱发丹参幼苗叶片保卫细胞内Ca2+迸发，持续时间为2~3 min，丹参幼苗丹酚酸B生物合成量亦显著增加，且丹酚酸B合成量的增加发生在Ca2+迸发之后。胞外Ca2+通道抑制剂、胞内Ca2+通道抑制剂以及胞内钙调素拮抗剂均可抑制水杨酸诱导的Ca2+迸发和丹酚酸B的生物合成。结果表明水杨酸诱发的Ca2+对丹参幼苗丹酚酸B生物合成具有重要的调控作用。

Abstract:

In order to study the effects of Ca2+ in the biosynthesis of salvianolic acid B (Sal B) induced by salicylic acid (SA) in the young seedlings of Salvia miltiorrhiza, we used confocal laser scanning microscopy and high performance liquid chromatography to measure the change of relative fluorescence intensity of Ca2+ and the contents of Sal B induced by SA before and after the application of extracellular calcium channel inhibitors (VP and LaCl3), intracellular calcium channel inhibitor (LiCl), as well as intracellular calmodulin antagonist (TFP). SA could induce the calcium burst, and the Ca2+ peak could last to 2–3 min in the guard cells of S. miltiorrhiza, which prompted the biosynthesis of Sal B after the Ca2+ burst. Both Vp or LaCl3, and LiCl or TFP could inhibit the burst of Ca2+ and the biosynthesis of Sal B. The above results demonstrated that Ca2+ from the extracellular and the intracellular calcium store regulate the biosynthesis of Sal B elicited by salicylic acid in S. miltiorrhiz young seedlings.