不同于体细胞，哺乳动物的卵母细胞具有极性，导致其独特的不均等减数分裂。这种不均等分裂对于卵胞质内的营养和遗传物质的保存是至关重要的，直接影响到后期的受精以及胚胎发育。到现在为止，对于卵母细胞不均等分裂的分子机制了解的还很少。之前的工作证明微丝直接参与了卵母细胞的极性形成。而我们前期的研究证明微丝相关蛋白Arp2/3复合物参与了这一过程，但是，还不清楚G蛋白酶相关效应因子是否参与了哺乳动物卵子的不均等分裂。为了研究G蛋白酶相关因子在卵母细胞极性形成过程中的功能和机制，本项目将采用RNA干扰、过表达、基因敲除等技术手段，结合活细胞工作站观察，深入研究G蛋白酶Cdc42效应因子LIMK和Cofilin在小鼠卵子纺锤体迁移和定位，极性产生、极体排出等过程中的功能，并阐明其作用机制和信号通路，进一步拓展对卵母细胞极性产生的认识，为卵子质量控制、受精及后期胚胎发育的调控提供理论基础。

Different from somatic cells, mammalian oocyte has polarity, which results in a unique asymmetric meiotic division. This asymmetry is critical for the retention of maternal components, successful fertilization, and early embryo development. Till now, the understanding about the molecular mechanism of oocyte asymmetric division is still limited. Previous work showed that actin is directly involved in the formation of oocyte polarity. Our previous work also showed that actin related protein Arp2/3 complex regulated this process. However, it is still unclear whether GTPase effector involves in this unique cell division. To explore the functions and related mechanisms of GTPase effector on the formation of oocyte asymmetry, we will employ RNAi, overexpression, and knock out approches, together with time lapse microscopy to investigate the roles of GTPase Cdc42 effector LIMK and Cofilin on the spindle migration and positioning, polarity formation and polar body extrusion in mouse oocytes. This study will help us furthur understand the mechanism of oocyte polarity formation and provide the support for oocyte quality control, sucessful fertilization and following early embryo development.