转录因子SALL4是体细胞重编程体关键因子之一，但SALL4调控多能性网络重建的机制尚未阐明。我们前期建立了以SALL4为主的非Yamanaka因子体细胞重编程体系，生物信息学分析提示SALL4可能影响pre-mRNA可变剪接过程。pre-mRNA可变剪接参与调控早期胚胎发育、细胞分化、体细胞重编程等多种细胞命运决定过程。因此，我们猜想SALL4可能通过调控可变剪接影响体细胞重编程。本研究拟以非Yamanaka因子将MEF诱导为iPSC为细胞模型，采用RNA-seq、ChIP-seq和体外荧光报告系统等技术，验证多能性重建过程中SALL4对可变剪接因子调控作用，鉴定剪接因子调控的下游基因并揭示其在重编程过程中作用，进而阐明SALL4调控体细胞重编程的分子机制，本研究将为揭示重编程机制提供新的视角，有助于理解细胞命运决定调控规律。

The transcription factor SALLl4 play a critical role for reprogramming, but its regulatory role during iPSC induction remain to be elucidated. We established a non-Yamanaka factor somatic reprogramming system based on Sall4. Bioinformatics analysis suggested that SALL4 regulates pre-mRNA splicing process during reprogramming. Pre-mRNA alternative splicing affects many cell fate decision processes such as early embryonic development, cell differentiation, and somatic reprogramming. Therefore, we hypothesis that SALLl4 may affect somatic reprogramming by regulating alternative splicing. In this study, we will use RNA-seq, ChIP-seq, and in vitro fluorescence reporter system to verify alternative splicing genes, splicing factors regulated by SALL4, explore the molecular mechanism of SALL4 by regulation pre-mRNA alternative splicing. Integrated analyses the regulatory networks underlying somatic cell reprogramming will improve our understanding of cell fate decisions.