本研究旨在证实Fad24作为DFAT细胞的成脂再分化和成肌转分化的共性开关蛋白，受不同上游转录因子KLFs家族成员的调控，引起转录后修饰和活性不同，对下游靶基因的选择和功能不同，使DFAT细胞向不同方向分化。研究拟采用细胞培养、诱导分化、免疫细胞化学、荧光共聚焦显微镜、荧光定量RT-PCR、外源基因转染、启动子活性部位5'端系列删除及定点突变、双荧光素酶报告基因及染色质免疫共沉淀等技术进行分析。通过研究拟阐明三个问题：在两种不同分化途径中，不同KLFs调控Fad24表达模式的功能差异；不同KLFs调控引起的Fad24对下游靶基因的选择与调控的功能差异；Fad24基因启动子上不同KLFs的结合位点及它们直接结合。这些研究结果将揭示DFAT细胞再分化和转分化启动的转录调控机制，能够为脂肪组织的再分化和转分化调控奠定理论基础。

This research aims to confirm that Fad24, a common switch protein for adipogenic redifferentiation and myogenic transdifferentiation of DFAT cells and regulated by the different upstream transcription factors of the KLFs family members, can cause the differences of the modifications and activities post-translation and the choices and functions of downstream target genes, and make the DFAT cells differentiation in different directions. This study will apply cell culture, induced differentiation, immunocytochemistry, confocal fluorescence microscope, fluorescence quantitative RT-PCR, exogenous gene transfection, a series of 5-deletions and fixed point mutations of promoter activity region, dual luciferase report gene assay and chromatin immunoprecipitation to clarify three issues: the different function of KLFs to regulate Fad24 expression pattern in two different differentiation pathways; the different function of Fad24 regulated by different KLFs to choose and regulate downstream target genes; and the different KLFs binding sites on the Fad24 gene promoter and their direct combination. These results will reveal the transcription regulation mechanism in DFAT cell redifferentiation and transdifferentiation and lay a theoretical foundation for adipose tissue redifferentiation and transdifferentiation.