Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Enhancer profiling in Esrrb-/- ES cells [4C-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: GSE139187 | GEO | 2019/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

2019-12-31 | GSE129179 | GEO

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

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

| PRJNA578716 | ENA

Enhancer profiling in Esrrb-/- ES cells

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

| PRJNA578710 | ENA

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. ChIP experiments were carried out with chromatin prepared from E14 cells as previously described (Stock et al., 2007), using 8-10 ug primary antibody for NcoA3 and 600 ug pre-cleared chromatin per IP. Antibody for NcoA3 was from Santacruz (sc-9119) .

2012-10-02 | E-GEOD-37262 | biostudies-arrayexpress

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

2012-10-02 | GSE37262 | GEO

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

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

| PRJNA530398 | ENA

Epigenetic modulation of a hardwired 3D chromatin landscape in two naive states of pluripotency. (4C-seq)

Project description:The mechanisms underlying enhancer activation and the extent to which enhancer-promoter rewiring contributes to spatiotemporal gene expression are not well understood. Using integrative and time resolved analyses we show that the extensive transcriptome and epigenome resetting during the conversion between ‘serum-’ and ‘2i’-states of mouse embryonic stem cells (ESCs) takes place with minimal enhancer-promoter rewiring that becomes more evident in primed-state pluripotency. Instead, differential gene expression is strongly linked to enhancer activation via H3K27ac. Conditional depletion of TFs and allele-specific enhancer analysis reveals an essential role for Esrrb in H3K27-acetylation and activation of 2i-specific enhancers. Restoration of a polymorphic ESRRB motif using CRISPR/Cas9 in a hybrid ESC-line, restores ESRRB binding and enhancer H3K27ac in an allele-specific manner but has no effect on chromatin interactions. Our study shows that enhancer activation in serum- and 2i-ESCs is largely driven by TF-binding and epigenetic marking in a hardwired network of chromatin interactions.

2019-04-30 | GSE113750 | GEO

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.

2022-10-12 | GSE199613 | GEO

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

2022-10-12 | GSE199612 | GEO

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

2022-10-12 | GSE199609 | GEO