中文摘要：

以野生型和hy4突变体拟南芥为材料，运用药物学方法研究可能参与蓝光诱导叶片花色素苷积累和CHS基因表达的信号组分。培养基中外施Ca^2＋、钙离子通道剂A23187、螯合剂EGTA、钙通道阻断剂尼群地平（nifedipine，Nil）以及异博定（verapermil）的实验证实，蓝光诱导13d龄叶片花色素苷积累和CHS基因表达需要胞外Ca^2＋的参与，而蓝光作用是由cryl（crypmchromel）介导的。此外，质膜黄素蛋白抑制剂DPI（diphenylene iodonium）抑制蓝光诱导的花色素苷积累，质膜H^＋ -ATPase激活剂壳梭胞素（fusicoccin，FC）抑制蓝光反应，而抑制剂钒酸钠则起促进作用。CaM拮抗剂w7、Ca^2＋ -ATPase抑制剂EB（erythrosine B）、G蛋白激活剂霍乱霉素（cholera toxin，CTX）以及抑制剂百日咳毒素（pertussis toxin，PTX）对蓝光下野生型与hy4的花色素苷积累都有影响。对药物实验的分析表明，质膜氧化还原系统、H^＋ -ATPase可能参与依赖于外源Ca^2＋的蓝光反应。

英文摘要：

Previous research demonstrated that blue light （BL）（50 μmol m^-2 s^-1） induced anthocyanin accumulation in 13-day old Arabidopsis seedling. In this studies, a sets of pharmacological experiments were conducted to evaluate weather the influx of extracellular Ca^2＋ and the membrane components were involved in blue light induced anthocyanin accumulation and CHS gene expression. When the seedlings were cultured on the B5 medium with or without Ca^2＋, A23187, EGTA, nifedipine （Nit）, verapermil, the changes of anthocyanin accumulation induced by BL were determined. It was found that the extracellular Ca^2＋ was required for the BL induced pigmentation and the CHS gene expression and cryl is one of the main photoreceptors mediating the BL response. DPI, an inhibitor of plasma membrane （PM） flavoenzymes, inhibited the BL response in WT leaves. FC, an activator of PM H^＋-ATPase showed the inhibition of BL induced anthocyanin accumulation whereas vanadate, an inhibitor of the H^＋-ATPase had promoting effect. Moreover, W7 （N- （6-aminohexyl）-5-chloro-1- naphthalenesulfonamide）, an antagonist of calmodulin, erythrosine B （EB）, an inhibitor of the Ca^2＋-ATPase, cholertha toxin （CTX）, a G protein activator and pertussis toxin （PTX）, a G protein inhibitor were all affected the anthocyanin accumulation induced by BL both in WT and in hy4 leaves. The results suggested that PM redox system, H^＋-ATPase are involved in the Ca^2＋ dependent BL induction of anthocyanin accumulation in the leaves of A rab idopsis.