腭中嵴上皮细胞形态的改变，特别是表面丝状伪足的形成与消失与腭突的融合有着密切的关系。本研究基于同源器官发育初期具有类似的发育图式的特点和前期研究结果，认为CDH23可能通过协同Harmonin蛋白控制腭中嵴上皮细胞丝状伪足的粘附而参与调节腭突的融合，进而影响腭的发育。为此，同时利用条件性基因敲除，RNAi,timelap, confocal,x-gal及相关分子生物学技术从细胞，器官，母体环境不同层面，多个角度，观察腭中嵴上皮细胞形态，丝状伪足与腭融合的关系，通过检测CDH23，Harmonin, E-cadherin 及PAR/aPKC的时空表达改变来探讨可能的内在分子机制，并利用综合征和非综合征性唇腭裂的基因样本库，采用单核苷酸多态性分析方法来判断CDH23基因与腭裂的关联性和贡献率，从而为腭的发育以及非综合征性腭裂这一常见先天性畸形的防治提供新的理论依据.

Cleft palate is a common congenital malformation.The shape of Palatal medial epithelial cells plays important role in palatal fusion. As both palate and ear come from the ectoderm during embryonic development, we though that CDH23 and Harmonin may synergistically regulate palatal fusion by modulating filopodia adhesion.We'll use conditional gene knockout, RNAi, timelap, confocal, x-gal and other molecular biological techniques to show how the palatal crest epithelial cell's filopodia works during palatal fusiong in by cell and organ culture. Through detecting spatial and temporal expression of CDH23, Harmonin, E-cadherin and of PAR/aPKC , we'll understand the intrinsic molecular mechanism of palatal fusion. To further explore the possible genetic co-relation between cleft palate and CDH23, we use single nucleotide polymorphism analysis to determine the contribution of CDH23 gene to cleft palate. Then, we may reveal a new molecular theoretical basis for the development of cleft palate, and provide new theory for biological treatment of non-syndromic cleft palate.