树突在神经系统信息交流及神经环路的形成中具有重要作用，很多神经系统疾病的发生都与树突结构缺陷相关，比如精神分裂症、自闭症、Rett综合症、唐氏综合症等，树突结构正确发育对神经系统的结构功能具有重要意义。然而关于树突发育的分子机制依然知之甚少，因此选择合适的模型对树突形态发生进行研究具有重要意义。秀丽隐杆线虫（C. elegans）PVD神经元具有类似于哺乳动物神经元的复杂多级分支状结构，是很好的研究树突发育的模型。种间保守的细胞间紧密连接（tight junction）组分HPO-30/claudin可以调控PVD树突发育，然而分子机制并不清楚。我们将以线虫PVD树突为模型，采用遗传学，分子生物学，细胞生物学，生物化学，结构生物学等方法对HPO-30调控树突发育机制进行研究，以期为高等动物树突发育机制和相关疾病的研究提供借鉴。

Dendrites play an important role in the formation of neural circuits and information exchange among neurons. Malfunction of dendrites causes neurological disorders, such as schizophrenia, autism, Rett syndrome and Down's syndrome. The normal function of dendrites is essential for the neuron system. However, the mechanism of dendrite morphogenesis is still not very clear. Here, we use C. elegans PVD neurons, which have many complex branches similar to mammalian neurons, as the model system to study dendrite morphogenesis. The conserved tight junction component HPO-30/claudin controls PVD dendrite development, but the mechanism is still unknown. We will use genetics, molecular biology, cell biology, biochemistry and structural biology assays to study the regulatory mechanism of HPO-30/claudin. This study will shed light on the mechanism of dendrite development and related dendrite diseases in mammals.