常染色体显性多囊肾病是最常见的致死性遗传性肾病，由PKD1和/或PKD2基因突变所致，发病机制未完全阐明，缺乏有效治疗手段。我们前期研究发现，敲低斑马鱼pkd2基因表达可降低PC2、Scribble及磷酸化YAP表达；过表达Scribble及磷酸化YAP可降低pkd2缺失斑马鱼胚胎的囊肿比例；Scribble可调控YAP的磷酸化水平，影响囊肿形成。据此，我们提出PC2-Scribble-YAP通路在多囊肾病囊肿形成中发挥作用这一新的机制假说。我们利用激光共聚焦和免疫共沉淀等技术研究Scribble与PC2的相互作用；运用显微注射和斑马鱼突变体构建等技术探究Scribble对YAP磷酸化的调控；采用药物干预实验研究提高磷酸化YAP水平干预多囊肾病的作用。最终阐明PC2-Scribble-YAP通路在多囊肾病囊肿发生发展中的重要作用及机制，为寻找治疗多囊肾病的全新靶标提供理论和实验依据。

Autosomal dominant polycystic kidney disease (ADPKD) is the most common fatal hereditary kidney disease caused by mutations in PKD1 and/or PKD2 genes. However, the pathogenesis of the disease is still unclear and there is no effective treatment for it. In our previous studies, we found that knockdown of pkd2 in zebrafish embryos (pkd2 morphants) would decreased the expression of PC2, Scribble and phosphorylated YAP; overexpression of Scribble and phosphorylated YAP could reduce cyst formation in pkd2 morphants; Scribble could regulate YAP phosphorylation to influence the cyst formation. Accordingly, we propose a new mechanism hypothesis that the PC2-Scribble-YAP pathway plays an important role of in regulating cyst formation in ADPKD. In this study, we used the techniques of confocal microscopy and co-immunoprecipitation to identify the interaction between Scribble and PC2, investigated the role of Scribble in regulating the phosphorylation of YAP by using microinjection and zebrafish mutational analyses, and explored the role of YAP phosphorylation in the treatment of ADPKD. Thus, we will elucidate the effect and a novel mechanism of the PC2-Scribble-YAP pathway in the cyst formation of ADPKD, which may provide a new potential therapeutic target for ADPKD.