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Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [RNA-Seq]

ABSTRACT: Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [RNA-Seq]

PROVIDER: PRJNA558468 | ENA |

REPOSITORIES: ENA

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Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [ChIP-Seq]

Project description:Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [ChIP-Seq]

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Enhancer RNAs mediate estrogen-induced decommissioning of selective enhancers by recruiting ER and its cofactor

Project description:Enhancer RNAs mediate estrogen-induced decommissioning of selective enhancers by recruiting ER and its cofactor

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Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [RNA-Seq]

Project description:Estrogen receptor alpha (ERα) signaling mainly occupies on distal enhancers within genome and plays an essential role in ERα-positive breast cancer. ERα usually requires co-factors to regulate the enhancer activity. By analysis of genome-wide nascent transcript profiling in breast cancer cells, we identified a special group of eRNAs that are functionally important for estrogen-induced transcriptional repression. In addition to stabilizing promoter-enhancer looping structure, these eRNAs recruit ERα to particular enhancers of target genes, facilitate the hierarchical formation of a functional transcriptional complex, and cause gene silencing. Interestingly, we found that ERα directly binds to eRNAs and its DNA-binding domain mediates the interaction with RNA molecules. Our ChIP-seq data in MCF-7 cells indicating that ERαwas not able to bind to E2-activated enhancers, which is consistent with the DNA-binding function reported before; moreover the DBD-truncated ERα was not able to bind to E2-repressed enhancers as well, which further supports our hypothesis that eRNA from E2-repressed enhancers help to recruit ERα to specific enhancers through the interaction with DBD domain. Substitution of ERα-DDBD showed a global effect on both induction and repression of ERα target genes as examined by RNA-seq. Further, these eRNAs help with the formation of a specific ERα-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses transcription of target genes. Our work demonstrated that eRNAs, as a distinctive class of cis-acting molecules besides chromatin regulatory elements, play an important role in modulating and refining locus-specific transcriptional program.

2020-06-23 | GSE135339 | GEO

Enhancer RNA mediate estrogen-induced transcriptional repression by recruiting ERa and its cofactor to selective enhancers [ChIP-Seq]

2020-06-23 | GSE135340 | GEO

Enhancer RNAs Mediate Estrogen-Induced Decommissioning of Selective Enhancers by Recruiting ERα and Its Cofactor.

Project description: Not available

| S-EPMC8564762 | biostudies-literature

Enhancer RNAs mediate estrogen-induced decommissioning of selective enhancers by recruiting ER and its cofactor

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

2020-06-23 | GSE135341 | GEO

Estradiol Induced Transcriptional Profile of EAAE DNA Binding Deficient ERa Uterus

Project description:To evaluate the ability of a DNA binding deficient ERa to mediate transcriptional responses in the mouse uterus, ovariectomized mice were injected with 100 ul of saline or 250 ng of estradiol (E2) in 100 ul saline, uterine tissue was collected 2 hours filllowing the injection, and RNA was isolated

2015-03-24 | GSE56423 | GEO

Ligand dependent gene regulation by transient ERa clustered enhancers

Project description:Unliganded Estrogen receptor alpha (ERa) has been implicated in ligand-dependent gene regulation. Upon ligand exposure, ERa binds to several EREs relatively proximal to the pre-marked, or persistent, ERa-bound sites and affects transient but robust gene expression. However, the underlying mechanisms are not fully understood. Here we demonstrate that upon ligand stimulation, persistent sites interact extensively, via chromatin looping, with the proximal transiently ERa-bound sites, forming Ligand Dependent ERa Enhancer Cluster in 3D (LDEC). The E2-target genes are regulated by these clustered enhancers but not by the H3K27Ac super-enhancers. Further, CRISPR-based deletion of TFF1 persistent site disrupts the formation of its LDEC resulting in the loss of E2-dependent expression of TFF1 and its neighboring genes within the same TAD. The LDEC overlap with nuclear ERa condensates that coalesce in a ligand and persistent site dependent manner. Furthermore, formation of clustered enhancers, as well as condensates, coincide with the active phase of signaling and their later disappearance results in the loss of gene expression even though persistent sites remain bound by ERa. Our results establish a direct link between ERa condensates, ERa enhancer clusters, and transient, but robust, gene expression in a ligand-dependent fashion.

2019-11-22 | GSE136302 | GEO

Transcription profiling of mouse ERa abalated differentiated osteoclasts

Project description:Estrogen clearly prevents osteoporotic bone loss by attenuating bone resorption. The molecular basis of how this is accomplished, however, remains elusive. Here we report a critical role of osteoclastic ERa in mediating estrogen action on bone in females. We selectively ablated ERa in differentiated osteoclasts (ERa dOc/dOc). ERa dOc/dOc females, but not males, exhibited clear trabecular bone loss, similar to the osteoporotic bone phenotype in post-menopausal women. Recovery of bone loss by estrogen treatment of the ovariectomized ERa dOc/dOc females was ineffective in the trabecular areas of the long bones and lumbar vertebral bodies. Osteoclastic apoptosis, induced by estrogen, occurred simultaneously with up-regulation of Fas ligand (FasL) expression in intact trabecular bones of ERa +/+mice, but not in ERa dOc/dOc mice. ERa was also required for similar effects of estrogen and tamoxifen in cultured osteoclasts. These findings suggest that the osteoprotective actions of estrogen and SERMS are mediated at least in part through osteoclastic ERa in trabecular bone; and the life span of mature osteoclasts is regulated through activation of the Fas/FasL system. Experiment Overall Design: Wild type and osteoclast-specific Estrogen Receptor alpha knock-out mice were ovariectomized. The number of both genotypes of mice was eight. The mice of each genotypes were divided to vehicle control and estrogen treated group. Four hours after chemical treatment, the distal 5 mm of the left femurs were harvested after sacrificing by cervical dislocation and total RNAs were purified for Affymetix GeneChip microarray analysis without pooling. Therefore, this experiment consists of four groups with four replicates per group.

2008-06-15 | E-GEOD-7798 | biostudies-arrayexpress

Discovery of Selective Estrogen Receptor Covalent Antagonists (SERCAs) for the treatment of ERa(WT) and ERa(MUT) breast cancer.

Project description:Discovery of Selective Estrogen Receptor Covalent Antagonists (SERCAs) for the treatment of ERa(WT) and ERa(MUT) breast cancer.

| PRJNA475560 | ENA

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