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Homo sapiens

ABSTRACT: Multiplex Enhancer Interference Reveals Collaborative Control of Gene Regulation by Estrogen Receptor Alpha Bound Enhancers [ChIP-Seq]

PROVIDER: PRJNA390058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5666340.fastq.gz	Fastqsanger.gz
	SRR5666341.fastq.gz	Fastqsanger.gz
	SRR5666342.fastq.gz	Fastqsanger.gz
	SRR5666343.fastq.gz	Fastqsanger.gz
	SRR5666334.fastq.gz	Fastqsanger.gz

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

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Project description:Multiplex Enhancer Interference Reveals Collaborative Control of Gene Regulation by Estrogen Receptor Alpha Bound Enhancers [RNA-Seq]

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Regulatory Sharing Between Estrogen Receptor α Bound Enhancers

Project description:Regulatory Sharing Between Estrogen Receptor α Bound Enhancers

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The SET Oncoprotein Promotes Estrogen-Induced Transcription by Facilitating Establishment of Active Chromatin

Project description:SET is a multifunctional histone-binding oncoprotein that regulates transcription by an unclear mechanism. Here, we show that SET enhances estrogen-dependent transcription. SET knockdown abrogates transcription of estrogen-responsive genes and their enhancer RNAs (eRNAs). In response to 17β-estradiol (E2), SET binds to the estrogen receptor α (ERα) and is recruited to estrogen receptor α (ERα)-bound enhancers and promoters at estrogen response elements (EREs). SET functions as a histone H2 chaperone that dynamically associates with H2A.Z via its acidic C-terminal domain and promotes H2A.Z incorporation, ERα, MLL1 and KDM3A loading and modulates histone methylation at EREs. SET depletion diminishes recruitment of condensin complexes to EREs and impairs E2-dependent enhancer-promoter looping. Thus, SET boosts E2-induced gene expression by establishing an active chromatin structure at ERα-bound enhancers and promoters, which is essential for transcriptional activation.

2023-02-01 | GSE200900 | GEO

The SET Oncoprotein Promotes Estrogen-Induced Transcription by Facilitating Establishment of Active Chromatin

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

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

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

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

| PRJNA613101 | ENA

Functional Importance of eRNAs for Estrogen-dependent Gene Transcriptional Activation

Project description:The functional importance of gene enhancers in regulated gene expression is well established. In addition to widespread transcription of long non-coding RNA (ncRNA) transcripts in mammalian cells, bidirectional ncRNAs referred to as eRNAs are present on enhancers. However, it has remained unclear whether these eRNAs are functional, or merely a reflection of enhancer activation. Here, we report that 17 ?-estradiol (E2)-bound estrogen receptor alpha (ER?) on enhancers causes a global increase in eRNA transcription on enhancers adjacent to E2 upregulated coding genes. These induced eRNAs, as functional transcripts, appear to exert important roles for the observed ligand-dependent induction of target coding genes, causing an increased strength of specific enhancer:promoter looping initiated by ER? binding. Cohesin, present on many ER?-regulated enhancers even prior to ligand treatment, apparently contributes to E2-dependent gene activation by stabilizing E2/ER?/eRNA-induced enhancer:promoter looping. Our data indicate that eRNAs are likely to exert important functions in many regulated programs of gene transcription. The ChIP-seqs in this study measure the binding landscape of master transcription regulator of estrogen signaling - ER?, together with common histone marks including H3K27ac and H3K4me1 in MCF7 cells. These data serve as the basis to understand the enhancer map and subsequent analysis of eRNA expression using GRO-seq. The GRO-seq measures the trancription of nascent RNAs in the genome. From MCF7 cells treated with veichle or estrodial, we could identify estrogen-regulated eRNAs and subsequently could study their functions.

2013-06-04 | E-GEOD-45822 | biostudies-arrayexpress

The histone variant H2A.Z is an important regulator of enhancer activity.

Project description:Gene regulatory programs in different cell types are largely defined through cell-specific enhancers activity. The histone variant H2A.Z has been shown to play important roles in transcription mainly by controlling proximal promoters, but its effect on enhancer functions remains unclear. Here, we demonstrate by genome-wide approaches that H2A.Z is present at a subset of active enhancers bound by the estrogen receptor alpha (ERα). We also determine that H2A.Z does not influence the local nucleosome positioning around ERα-enhancers using ChIP-sequencing at nucleosomal resolution and unsupervised pattern discovery. We further highlight that H2A.Z-enriched enhancers are associated with chromatin accessibility, H3K122ac enrichment and hypomethylated DNA. Moreover, upon estrogen stimulation, the enhancers occupied by H2A.Z produce enhancer RNAs (eRNAs), and recruit RNA polymerase II as well as RAD21, a member of the cohesin complex involved in chromatin interactions between enhancers and promoters. Importantly, their recruitment and eRNAs production are abolished by H2A.Z depletion, thereby revealing a novel functional link between H2A.Z occupancy and enhancer activity. Taken together, our findings suggest that H2A.Z acts as an important player for enhancer functions by establishing and maintaining a chromatin environment required for RNA polymerase II recruitment, eRNAs transcription and enhancer-promoters interactions, all essential attributes of enhancer activity. The MNase ChIP-seqs in this study measure the genome-wide binding landscape of H2A.Z, H3K4me1, H3K27ac and H3K4me3 in MCF-7 cells in the absence or presence of E2. Two biological replicates were done for each ChIP-seq experiment and for each condition, as well as, control input.

2015-08-31 | E-GEOD-57436 | biostudies-arrayexpress

Target Gene Repression Based on Dismissal of Polymerase II from Estrogen Receptor Trans-bound Enhancers Is Associated With Clinical Outcome in Human Breast Cancer [GRO-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 | GSE73957 | GEO

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