ZAP1 基因过表达转基因果蝇的构建与功能鉴定

微量金属元素锌稳态与帕金森病(Parkinson's disease, PD)的发生发展密切相关，酵母 ZAP1 转录因子已被鉴定可感知细胞锌状态，可通过增加其靶基因的表达以响应锌缺乏症，然而，ZAP1 与 PD 发生发展是否有关鲜有报道。为了更好地研究 ZAP1 的功能，文章利用聚合酶链式反应（polymerase chain reaction，PCR）扩增出 ZAP1 基因全长，并将其连接至 pUAST 上构建 pUAST-ZAP1；采用显微注射技术导入果蝇卵，获得 UAS-ZAP1 转基因果蝇，通过 PCR 验证了转基因果蝇构建成功；再利用遗传学和行为学方法研究转基因成功的果蝇在多巴胺能神经元中进行特异性表达的效果，发现过表达 ZAP1 能够挽救鱼藤酮诱导的果蝇攀爬、跳跃能力的降低。该研究结果为探究 ZAP1 基因在鱼藤酮诱导的 PD 模型中的功能奠定了基础。

The homeostasis of trace metal element zinc is closely related to the occurrence and development of Parkinson's disease(PD). The yeast ZAP1 transcription factor has been identified to perceive cellular zinc status and increase the expression of its target gene in response to zinc deficiency. However, there have been few reports on the relationship between ZAP1 and the occurrence and development of PD. In order to better study the function of ZAP1, this paper amplified the full length of the ZAP1 gene using polymerase chain reaction(PCR) and connected it to pUAST to construct pUAST-ZAP1. Drosophila eggs were introduced using microinjection technology to obtain UAS-ZAP1 transgenic Drosophila. The successful construction of the transgenic Drosophila was verified through PCR, and genetic and behavioral methods were used to specifically express the ZAP1 gene in dopaminergic neurons of the transgenic Drosophila. Overexpression of ZAP1 was found to rescue the reduced climbing and jumping ability induced by rotenone in Drosophila. These findings lay a foundation for further studying the function of ZAP1 gene in rotenone-induced PD.