减数分裂是生殖细胞特有的一种分裂方式，它是配子发生过程中的一个关键环节，目前已经成为生殖生物学和发育生物学领域的研究热点。阐明减数分裂调控的分子机制在基础理论和临床应用方面都具有非常重要的意义。Wdr62基因编码一个包含多个WD重复序列的蛋白，该基因突变导致人类原发性小头畸形（MCPH）。我们的前期研究发现Wdr62从胚胎E10.5天开始在生殖细胞中持续高表达。为了研究Wdr62在生殖细胞发育过程中的功能，我们制备了Wdr62的基因敲除小鼠模型。初步研究发现敲除Wdr62后导致雌性小鼠生殖细胞在胚胎E13.5天开始大量死亡，而雄性小鼠的生殖细胞在出生后3-5天丢失。进一步研究发现缺失Wdr62后生殖细胞不能启动减数分裂，提示该基因在减数分裂过程中发挥重要作用。本研究将利用基因敲除的小鼠模型，同时结合细胞和生化方法对Wdr62在生殖细胞减数分裂过程中的功能和作用机制进行系统研究。

Germ cells are unique in undergoing meiosis to generate oocytes and sperm. Currently, meiosis is one of hot topic in the field of reproductive biology and developmental biology. It is very important to elucidate the molecular mechanism of meiosis regulation in basic theory and clinical application. Wdr62 (WD40-repeat containing 62) gene encodes a protein with multiple WD40 repeats at the N-terminal， which contains 1523 amino acids . Mutation of Wdr62 is associate with autosomal recessive primary microcephaly (MCPH) in human patients. To investigate the functions of Wdr62 in germ cell development, we generated Wdr62 gene knockout mouse strain. Wdr62-deficient mice were grossly normal, but both males and females were infertile. Further studies revealed that massive germ cell loss was observed at E13.5 in Wdr62-deficient females. Whereas, germ cell loss was evident in males at 3 days after birth. We also found that the expression of meiosis related genes was completely absent in Wdr62-deficient germ cells in both males and females, suggesting that Wdr62 is involved in germ cell development by regulating meiosis initiation. In the present study, the physiological function and the molecular mechanism of Wdr62 in germ cell development and meiosis initiation will be explored using gene konckout mice model and other in vitro systems.