小鼠受精卵中微丝骨架的正确聚集和分布与早期细胞分裂关系密切。在此过程中参与的调控因子及信号调控机制目前尚不清楚。申请者研究发现过表达或敲低mTORC2和PKB/Akt都会影响小鼠受精卵微丝骨架聚集。结合文献报道PKB/Akt为mTORC2的底物蛋白。申请者分析mTORC2可能通过PKB/Akt蛋白发挥对微丝骨架分布的调控作用。而Girdin(girders of actin filaments)是一个新近发现参与微丝交联的PKB/Akt下游作用分子。研究显示PKB/Akt能够磷酸化Girdin蛋白，使其通过细胞骨架的重构在细胞迁移过程中扮演重要角色。综上分析如能证明mTORC2对Girdin蛋白的作用，则可提出：在小鼠受精卵早期发育中mTORC2通过PKB/Akt依赖的Girdin途径导致微丝骨架分布改变，促进受精卵早期分裂。为进一步阐明小鼠受精卵早期发育的分子机理提供新的思路和实验基础。

In mouse fertilized eggs, the proper assembly and distribution of actin cytoskeleton is intimately related with the cleavage of early-stage embryo..However, in mammals, especially in mouse fertilized eggs, the mechanisms and involved factors responsible for regulating the actin cytoskeleton are poorly defined. In our preliminary work, Both mTORC2 and PKB/Akt were found to modulate the division of mouse fertilized eggs through regulating the distribution of actin cytoskeleton. PKB/Akt has been proved to be a downstream target of the mTORC2 signaling pathway. Girdin, the newly found actin-cross linker, has been proved to be a downstream target of the Akt signaling pathway. Therefore, in this application, the expression of Girdin and its effect on F-actin organization in mouse fertilized eggs under the regulation of PKB/Akt will be tested by biological techniques..Collectively, this study aimed to prove the participation of mTORC2/Akt in F-actin assembling in early-stage cleavage of mouse fertilized eggs via the function of Girdin, which will provide novel thoughts and experimental basis for further clarifying the molecular mechanism(s) of actin dynamics in the development of mouse embryo.