The NuRD complex cooperates with SALL4 to orchestrate reprogramming

Author:

Wang Bo,Li Chen,Ming Jin,Wu Linlin,Fang Shicai,Huang Yi,Lin Lihui,Liu He,Kuang Junqi,Zhao ChengchenORCID,Huang Xingnan,Feng Huijian,Guo Jing,Yang Xuejie,Guo Liman,Zhang XiaofeiORCID,Chen JiekaiORCID,Liu JingORCID,Zhu Ping,Pei DuanqingORCID

Abstract

AbstractCell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. Here, we report that chromatin remodeling complex NuRD participates in closing open chromatin in the early phase of somatic reprogramming. Sall4, Jdp2, Glis1 and Esrrb can reprogram MEFs to iPSCs efficiently, but only Sall4 is indispensable capable of recruiting endogenous components of NuRD. Yet knocking down NuRD components only reduces reprogramming modestly, in contrast to disrupting the known Sall4-NuRD interaction by mutating or deleting the NuRD interacting motif at its N-terminus that renders Sall4 inept to reprogram. Remarkably, these defects can be partially rescured by grafting NuRD interacting motif onto Jdp2. Further analysis of chromatin accessibility dynamics demonstrates that the Sall4-NuRD axis plays a critical role in closing the open chromatin in the early phase of reprogramming. Among the chromatin loci closed by Sall4-NuRD encode genes resistant to reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, and may further illuminate chromatin closing as a critical step in cell fate control.

Funder

National Natural Science Foundation of China

Guangdong Science and Technology Department

Publisher

Springer Science and Business Media LLC

Subject

General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry,Multidisciplinary

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