子宫内膜作为与囊胚接触的第一道屏障结构，其上皮细胞发生一系列形态功能变化，包括极性重塑和离子通道的激活或抑制，以促进囊胚植入。课题组前期工作提示mTORC2成员Rictor在小鼠胚胎着床窗口期子宫内膜组织的表达增加，子宫内膜条件性敲除Rictor基因小鼠(Rictor d/d)表现为囊胚粘附失败，提示Rictor可能参与调控子宫内膜容受性的建立。研究表明，调控子宫内膜上皮细胞形态功能的关键因子Rac1和SGK1受到Rictor的调控。Rictor可通过磷酸化Akt促进Rac1的表达，通过磷酸化SGK1促进ENaC的功能。提示Rictor可能通过Akt/Rac1和SGK1/ENaC途径调控胚胎植入过程中子宫内膜上皮细胞的功能。本研究拟利用Rictor d/d小鼠模型，揭示在胚胎植入过程中Rictor调控子宫内膜功能的分子机制，通过细胞模型加以验证，为胚胎植入的分子调控机制提供新的思路。

The implantation of the blastocyst into the maternal uterus is a crucial step in mammalian reproduction. Endometrium epithelial cells are the first barrier to communicae with the blastocyst. A series of morphologic and functional transformation of endometrium epithelial cells, including polarity remodeling and activation or inhibition of ion channels, were essential during the implantation of the blastocyst. Our previous study found that the expression of Rictor which is a core subunit of mTORC2 in the endometrium increased accompanied with implantation of the blastocyst. Uterine-selective depletion of Rictor results in embryo implantation failure. That indicated Rictor may participated in the establishment of endometrial receptivity. Rac1 and SGK1, which play an important role in implantation, were regulated by Rictor. Rictor activates Rac1 by phosphorylating Akt. mTORC2/SGK1 is the key signal pathway to regulating the expression and function of. Therefore, Rictor may regulate the function of endometrial epithelial cells through Akt/Rac1 and SGK1/ENaC during embryo implantation. This study would employ the transgenic mice (Rictor d/d) to reveal the molecular mechanism by which Rictor regulating the function of endometrium during embryo implantation. The data would help improving the regulatory network of embryo implantation.