内质网（Endoplasmic Reticulum，简称ER）是真核细胞中由相互连通的片状（sheet）或管状（tubule）膜系统组成。ER在蛋白、脂类合成、钙储存、细胞凋亡等细胞学过程中发挥重要功能。ER形态的发生和维持非常重要，其形态的破坏将导致多种疾病如神经退行性疾病的产生。然而目前我们对ER庞大网络的形成和维持机制，尤其是神经元中ER形态和功能仍然缺乏深入认识，并且神经树突中ER形态功能研究主要集中于体外培养的细胞中，在体研究相对较少。本课题首先建立了秀丽隐杆线虫PVD神经元树突ER研究模型，并通过遗传筛选发现磷脂酰肌醇5-磷酸酶CIL-1对应基因突变影响PVD树突ER形态，具体作用机制未知，本课题将采用遗传学、细胞生物学、生物化学等研究方法深入研究其作用机制，预期研究结果将加深对神经树突ER发生的理解，也为相关疾病机制研究提供思路。

In eukaryotic cells, the endoplasmic reticulum (ER) is comprised of a network of sheets and tubules that form a continuous membrane system. It functions in many essential cellular processes, including protein synthesis, lipid synthesis, calcium storage, and apoptosis. ER morphogenesis and maintenance are very important, and many diseases such as neuronal degenerative diseases will happen if it is impaired. How the characteristic shape of the ER is established and maintained, especially in neuron dendrite is still not well-known. Most of neuronal dendrite ER morphology studies are from in vitro culture system, and in vivo study is lacking. In this project, we established an ER morphology study model using PVD dendrite of C. elegans. Furthermore, PI 5-Phosphatase mutant destroyed PVD dendrite ER morphology, while the mechanism is unknown. We will study the molecular mechanism of it using genetics, cell biology and biochemistry assay. It will deepen our understanding of ER morphogenesis in neuronal dendrite and provide new idea for the study of associated diseases.