DEPTOR是mTORC1和mTORC2复合物的重要组成部分，负调控mTOR自噬通路。近期研究表明，TSC2抑制mTORC1可以促进细胞重塑，提高体细胞重编程为诱导多能干细胞的效率；DEPTOR高表达于胚胎干细胞，提示其也可能直接调控干细胞多能性。但DEPTOR是否直接参与多能干细胞干性维持和体细胞重编程调控，尚不明确。结合本课题前期研究结果，本研究以兔干细胞为模型，拟采用RNA干涉、过表达和荧光霉素报告基因检测系统等技术手段，探讨DEPTOR维持兔胚胎干细胞多能性的作用及与其他多能性相关基因互作关系；重点探索DEPTOR-mTORC1在兔体细胞重编程中的作用，阐明DEPTOR调节自噬通路影响兔体细胞重编程的机理。本研究将为DEPTOR新功能的挖掘和自噬通路影响重编程效率的机理提供新见解。

DEPTOR is an important component of the mTORC1 and mTORC2 complexes, and is a negative regulator of mTOR pathway. Recent studies have shown that inhibition of mTORC1 complexes by TSC2 facilitated cell reshaping and promoted the reprogramming efficiency of somatic cells into induced pluripotent stem cells. DEPTOR is highly expressed in embryonic stem cells, suggesting that it may directly regulate pluripotent stem cells. However, whether DEPTOR is directly involved in stem cell maintenance and somatic reprogramming is not clear. According to our previous studies, rabbit stem cells were used as models in this study. RNA interference, gene over-expression, and luciferase reporter gene assay etc. will used to investigate the effect of DEPTOR on the rabbit pluripotent stem cells and the interaction with pluripotency-related genes. Meanwhile, we will explore the role of DEPTOR-mTORC1 in rabbit somatic reprogramming, and elucidate the mechanism by which DEPTOR regulates autophagy pathway in rabbit somatic cell reprogramming. This study will provide new insights into the new role of DEPTOR and the mechanism of the autophagy pathway affecting reprogramming efficiency.