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Regulatory Sharing Between Estrogen Receptor α Bound Enhancers [ATAC-seq]

ABSTRACT: Regulatory Sharing Between Estrogen Receptor α Bound Enhancers [ATAC-seq]

PROVIDER: PRJNA613100 | ENA |

REPOSITORIES: ENA

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Regulatory Sharing Between Estrogen Receptor α Bound Enhancers

Project description:Regulatory Sharing Between Estrogen Receptor α Bound Enhancers

| PRJNA613099 | ENA

Regulatory Sharing Between Estrogen Receptor α Bound Enhancers [ChIP-seq]

Project description:Regulatory Sharing Between Estrogen Receptor α Bound Enhancers [ChIP-seq]

| PRJNA613101 | ENA

Regulatory Sharing Between Estrogen Receptor α Bound Enhancers [ChIP-seq]

Project description:The human genome encodes an order of magnitude more gene expression enhancers than promoters, suggesting that most genes are regulated by the combined action of multiple enhancers. We have previously shown that neighboring estrogen-responsive enhancers, which are approximately 5,000 basepairs apart, exhibit complex synergistic contributions to the production of an estrogenic transcriptional response. Here we sought to determine the molecular underpinnings of the observed enhancer cooperativity. We generated genetic deletions of individual estrogen receptor  (ER) bound enhancers and found that enhancers containing full estrogen response element (ERE) motifs control ER binding at neighboring sites, while enhancers with pre-existing histone acetylation/accessibility confer a permissible chromatin environment to the neighboring enhancers. Genome engineering revealed that a cluster of two enhancers with half EREs could not compensate for the lack of a full ERE site within the cluster. In contrast, two enhancers with full EREs produced a transcriptional response greater than the wild-type locus. By swapping genomic sequences between enhancers, we found that the genomic location in which a full ERE resides strongly influences enhancer activity. Our results lead to a model in which a full ERE is required for ER recruitment, but the presence of pre-existing histone acetylation within an enhancer cluster is also needed in order for estrogen-driven gene regulation to occur.

2020-03-18 | GSE147141 | GEO

Regulatory Sharing Between Estrogen Receptor α Bound Enhancers [ATAC-seq]

2020-03-18 | GSE147140 | GEO

An Estrogen Receptor α-bound Human Chromatin Interactome

Project description:We developed Chromatin Interaction Analysis by Paired-End Tag sequencing (ChIA-PET) for de novo detection of global chromatin interactions, and comprehensively mapped the chromatin interaction network bound by estrogen receptor α (ERα) in the human genome. We performed 454 and Illumina sequencing analyses. Keywords: Epigenetics Using 454, we examined 3 libraries: IHM001 (Estrogen Receptor ChIA-PET), IHM043 (Estrogen Receptor ChIP-PET) and IHM062 (IgG ChIA-PET) Using Illumina, we examined 4 libraries: IHM001 (Estrogen Receptor ChIA-PET replicate 1, Paired End Sequencing), IHH015 (Estrogen Receptor ChIA-PET replicate 2, Paired End Sequencing), H3K4me3 ChIP-Seq and RNA polymerase II ChIP-Seq

2009-09-11 | E-GEOD-18046 | biostudies-arrayexpress

Multiplex Enhancer Interference Reveals Collaborative Control of Gene Regulation by Estrogen Receptor Alpha Bound Enhancers

Project description:Multiplex Enhancer Interference Reveals Collaborative Control of Gene Regulation by Estrogen Receptor Alpha Bound Enhancers

| PRJNA390054 | ENA

Regulatory Sharing Between Estrogen Receptor α Bound Enhancers

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-03-18 | GSE147142 | GEO

An Estrogen Receptor α-bound Human Chromatin Interactome

2009-09-11 | GSE18046 | GEO

Regulatory sharing between estrogen receptor ? bound enhancers.

Project description: Not available

| S-EPMC7337896 | biostudies-literature

Target Gene Repression Based on Dismissal of Polymerase II from Estrogen Receptor Trans-bound Enhancers Is Associated With Clinical Outcome in Human Breast Cancer [ChIP-seq]

Project description:We find that 17-β-estradiol (E2)-bound estrogen receptor α (ERα) is bound in trans to a cohort of FOXA1-dependent, constitutively activate enhancers, inactivating these enhancers by decommissioning/removing enhancer Polymerase II (Pol II), despite recruitment of coactivators. This is based on the surprising recruitment by the ERα DNA binding domain of the histone demethylase, KDM2A, which, functioning independently of its demethylase function. KDM2A mediates recruitment of NEDD4 complexes that ubiquitinate and dismisses Pol II from these "repressive" enhancers, resulting in the E2 down-regulated transcriptional program.

2019-09-04 | GSE73956 | GEO

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