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Enhancer profiling in Esrrb-/- ES cells [ChIP-seq]

ABSTRACT: We uncover a pivotal role for ESRRB in demarcating ESC-specific enhancer units, and propose that ESRRB’s developmentally-regulated extinction precipitates their decommissioning with impact on the rewiring of the pluripotency transcriptional programme upon embryo implantation

ORGANISM(S): Mus musculus

PROVIDER: GSE129179 | GEO | 2019/12/31

REPOSITORIES: GEO

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Enhancer profiling in Esrrb-/- ES cells [4C-seq]

Project description:We uncover a pivotal role for ESRRB in demarcating ESC-specific enhancer units, and propose that ESRRB’s developmentally-regulated extinction precipitates their decommissioning with impact on the rewiring of the pluripotency transcriptional programme upon embryo implantation.

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Enhancer profiling in Esrrb-/- ES cells

Project description:Enhancer profiling in Esrrb-/- ES cells

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A Nuclear Receptor Coactivator is Essential for Esrrb Activity and the Induction and Maintenance of the ES Cell State

Project description:Orphan nuclear receptor Esrrb is vital in maintaining ES cells and like Oct4, Sox2 and Nanog is essential for self-renewal and pluripotency. Esrrb functions in somatic cells via LBD/AF-2-dependent coactivator recruitment to target genes. Here we show that in ES cells coactivator recruitment is similarly required and identify Ncoa3 as the Esrrb coactivator needed for activation of its target genes. Ncoa3 is essential for self-renewal and the induction of pluripotency in reprogramming, and genome-wide analysis of Ncoa3 binding reveals extensive overlap with Esrrb and pluripotency factors along with marks of active genes. Mechanistically, we show Ncoa3 is specifically required to bridge RNApol2 to Esrrb. We thus identify a new member of the ES pluripotency network and describe Esrrb and Ncoa3 as key factors linking core pluripotency factors to the general transcription machinery.

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A Nuclear Receptor Coactivator is Essential for Esrrb Activity and the Induction and Maintenance of the ES Cell State

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Project description:Enhancer profiling in Esrrb-/- ES cells [ChIP-seq]

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

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

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Global gene-expression analyses of the Esrrb knockdown cells

Project description:In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming. Global gene expression effects of silencing the Esrrb gene. We used microarrays to detail the global programme of gene expression after silencing the Esrrb gene. Keywords: time-course Three biological replicates each for control GFP and Esrrb RNAi. The global gene expression profiles of the Esrrb knockdown cells were compared to control GFP knockdown cells for days 2, 4 and 6.

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