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NURD dependent Reprogramming by Sall4-Jdp2-Esrrb-Glis1 (ChIP-seq)

ABSTRACT: NURD dependent Reprogramming by Sall4-Jdp2-Esrrb-Glis1 (ChIP-seq)

PROVIDER: PRJNA820851 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR18507400_1.fastq.gz	Fastqsanger.gz
	SRR18507400_2.fastq.gz	Fastqsanger.gz
	SRR18507401_1.fastq.gz	Fastqsanger.gz
	SRR18507401_2.fastq.gz	Fastqsanger.gz
	SRR18507402_1.fastq.gz	Fastqsanger.gz

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NURD dependent Reprogramming by Sall4-Jdp2-Esrrb-Glis1 (RNA-seq)

Project description:Cell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. We report a system to reprogramming somatic cells to pluripotency by four factor combination (Sall4, Esrrb, Jdp2, Glis1). Mechanism study demonstrate that the Sall4-NuRD axis plays a critical role in the early phase of reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, may help establish early chromatin closing as a pre-requisite step in cell fate control.

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Project description:Reprogramming somatic cells to pluripotency represents a paradigm for cell fate determination. A binary logic of closing and opening chromatin provides a simple way to understand iPSC reprogramming driven by both Yamanaka factors or chemicals. Here we apply this logic to the design a four factor combination, Jdp2, Glis1, Essrb and Sall4 (4F), that reprogram MEFs to chimera competent iPSCs efficiently. RNA- and ATAC-seq reveal differences between JGES and 7F induced pluripotency, 7IP and JGES IP, in transcriptomic and chromatin accessibility dynamics(CAD). Sall4 emerges as a dominant force that can close and open chromatin with the help of Jdp2 and Glis1 in resetting somatic chromatin to a pluripotent state. These results reveal a previously unknown path between somatic and pluripotent states, open a door for cell fate control.

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