平面细胞极性（PCP）信号通路在上皮细胞平面极性的建立、细胞群的定向迁移等生物学过程中扮演着重要的角色。然而，关于PCP通路上游的细胞信号和PCP信号本身的调控机制，目前了解的仍然很少。我们前期的工作已表明，蛋白激酶Fused通过PCP通路的核心分子Prickle，参与了PCP信号的调控。我们推测Prickle蛋白的磷酸化修饰在PCP信号转导过程中发挥了重要功能，因此，本项目将开展以下研究：（1）确定Prickle的重要功能性磷酸化位点;（2）研究Fused上游的BMP信号或Hh信号与PCP信号通路之间的交叉整合特点;（3）探索出生缺陷相关的Prickle突变位点与其自身磷酸化及PCP信号转导的关系。本项目将进一步加深我们对平面细胞极性形成的分子机制的认识，为实现在源头上揭示相关出生缺陷疾病的遗传和诱发机制提供理论基础和新思路。

Planar cell polarity (PCP) pathway plays a key role in the directional cell migration and the alignments of cells within epithelium sheet. However, the upstream cues and the regulation of PCP signaling in these processes remain to be elucidated. Our previous works showed that a serine/threonine kinase, Fused (Fu) targets Prickle to participate in PCP pathway, so we hypothesize that the phosphorylation of Prickle may funtion as an important role in PCP signalling. Thus, it is very necessary to perform this project wih the following aims. 1) to determine the functional phosphorylated sites in Prickle; 2) to characterize the crosstalk between the BMP or Hh signaling upstream of Fused and PCP pathway; 3) to explore the relationship between the causality of Prickle variant in birth defect and its phosphorylation state. This project will not only provide insights into the mechanisms about PCP signaling, but also help us to better understand the etiology of PCP related birth defects in human.