哺乳动物卵母细胞成熟是一种独特的不均等分裂。在成熟过程中纺锤体迁移并定位至卵母细胞皮质，最终建立极性。卵母细胞极性降低或丧失能够导致均等分裂和多倍体卵子，直接影响卵母细胞成熟和受精率。但到目前为止，对调节卵母细胞极性形成的关键因子及其分子机制了解的并不多。本项目将探索和证明囊泡运输相关GTP酶Rab35是一种新的极性调节因子，拟通过RNA干扰、基因过表达及活细胞工作站等技术探索其对小鼠卵母细胞纺锤体迁移和定位，极性形成，微丝的表达和分布及不均等分裂的调控作用，并在此基础上深入探索Rab35作用的分子机制和建立其调控卵母细胞极性的完整分子信号通路。本研究将拓展对卵母细胞极性形成和不均等分裂分子调控机制的认识，并为全面了解卵子极性影响卵母细胞质量和雌性生殖奠定重要的理论基础。

Mammalian meiotic maturation is characterized by a unique asymmetric division. The asymmetry is ensured by the migration and the anchoring of the spindle to the cortex. In addition, the establishment of polarity is necessary for the extrusion of small polar bodies. Oocyte polarity reduction or loss will cause the production of symmetric and polyploidy eggs and results in abnormal oocyte maturation and reduced fertilization efficiency. However, till now, the critical regulators and their molecular regulatory mechanisms remain to be discovered. In this study, we will investigate if the vesicle transport-related GTPase Rab35 is a novel regulator of oocyte polarity. Using RNA interference, overexpression and time-lapse microscopy, we will explore the regulatory roles of Rab35 on spindle migration and positioning, mouse oocyte polarity formation, actin expression and distribution as well as asymmetric division, and we will also investigate the mechanisms and establish the molecular signaling pathway for the regulation of oocyte polarity. This study will provide further understanding on molecular mechanisms of oocyte polarity formation and asymmetric division, and will establish a pivotal theoretical foundation for clarifying the effects of polarity on oocyte quality and female reproductive.