作者
Bo Wang,Linlin Wu,Dongwei Li,Yuting Liu,Jing Guo,Chen Li,Yuxiang Yao,Yaofeng Wang,Guoqing Zhao,Xiaoshan Wang,Meijun Fu,He Liu,Shangtao Cao,Chuman Wu,Shengyong Yu,Chunhua Zhou,Yue Qin,Junqi Kuang,Ming Jin,Shilong Chu,Xuejie Yang,Ping Zhu,Guangjin Pan,Jiekai Chen,Jing Liu,Duanqing Pei
摘要
Highlights•Jdp2, Jhdm1b, Mkk6, Glis1, Nanog, Esrrb, and Sall4 (7F) convert MEFs into iPSCs•RNA-seq and ATAC-seq reveal a distinct path for 7F reprogramming•7F cooperate to open and close chromatin during 7F reprogramming•7F activate a TF network to induce pluripotencySummaryReprogramming somatic cells to pluripotency by Oct4, Sox2, Klf4, and Myc represent a paradigm for cell fate determination. Here, we report a combination of Jdp2, Jhdm1b, Mkk6, Glis1, Nanog, Essrb, and Sall4 (7F) that reprogram mouse embryonic fibroblasts or MEFs to chimera competent induced pluripotent stem cells (iPSCs) efficiently. RNA sequencing (RNA-seq) and ATAC-seq reveal distinct mechanisms for 7F induction of pluripotency. Dropout experiments further reveal a highly cooperative process among 7F to dynamically close and open chromatin loci that encode a network of transcription factors to mediate reprogramming. These results establish an alternative paradigm for reprogramming that may be useful for analyzing cell fate control.Graphical abstract