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Genome binding/occupancy profiling of ESRRA in the small intestinal epithelium

ABSTRACT: Genome binding/occupancy profiling of ESRRA in the small intestinal epithelium

PROVIDER: PRJNA1123752 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29402087_1.fastq.gz	Fastqsanger.gz
	SRR29402087_2.fastq.gz	Fastqsanger.gz
	SRR29402088_1.fastq.gz	Fastqsanger.gz
	SRR29402088_2.fastq.gz	Fastqsanger.gz
	SRR29402089_1.fastq.gz	Fastqsanger.gz

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Genome binding/occupancy profiling of ESRRA in the small intestinal epithelium

Project description:Amidst the obesity epidemic and advancements in satiety-targeting therapies, the transcriptional control of energy metabolism is crucial for managing obesity. The transcription factor Estrogen-related receptor α (ESRRA) regulates genes involved in mitochondrial biogenesis, gluconeogenesis, oxidative phosphorylation, and fatty acid metabolism. Although not essential for basic cellular function, ESRRA is vital for energy supply during physiological and pathological challenges. Studies show Esrra mutant mice have impaired fat metabolism and absorption, with germline Esrra loss conferring resistance to high-fat diet (HFD)-induced obesity. However, these studies often overlook tissue-specific roles. Esrra knockdown in the medial pre-frontal cortex reduces feeding and HFD-induced obesity, indicating possible neurological involvement. Notably, ESRRA is highly expressed in the gastrointestinal (GI) tract, a key player in dietary lipid metabolism and target of weight loss therapies.This study aims to investigate the impact of intestinal ESRRA and determine whether it contributes to resistance to diet-induced obesity.

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Transcriptomic changes upon ESRRA loss in the small intestinal epithelium

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Transcriptomic changes upon ESRRA loss in the small intestinal epithelium

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Project description:The mechanisms driving gene expression changes during intestinal differentiation are unclear. Our studies have shown differential recruitment and occupancy of Pol II to be a major driver of these gene expression changes. Additionally, we have identified the transcription factor HNF4 as a key player in shaping this phenomenon. To gain insights into the protein-based mechanisms underlying HNF4-mediated Pol II recruitment, we performed RIME (Rapid Immunoprecipitation Mass Spectrometry of Endogenous proteins) using anti-HNF4A antibodies in primary mouse epithelium.

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Targeting adipocyte ESRRA promotes osteogenesis and vascular formation in adipocyte-rich bone marrow

Project description:Extensive bone marrow adipocytes (BMAds) accumulation occurring under diverse pathophysiological conditions leads to bone deterioration.Estrogen-related receptor α (ESRRA) is a key regulator responding to metabolic stress.To explore the transcriptional role of ESRRA in regulating BMAds autonomous genes，bulk RNA-seq transcriptome analysis was performed in adipocyte-specific ESRRA deficiency BMAds lineage cells at 7 days upon adipogenic induction.

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Project description:To investigate the genetic loci bound by MafB in the intestinal epithelium, we used CUT&RUN.

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Nuclear receptor ESRRA promotes ERa-positive breast cancer through dual action on super enhancers and promoters to regulate gene transcriptional programs

Project description:ESRRA (Estrogen-Related Receptor Alpha) is an orphan nuclear receptor that plays a pivotal role in regulating cellular metabolism, mitochondrial biogenesis, and energy homeostasis through gene transcriptional control. It has been implicated in various physiological processes and diseases, including cancer. However, the transcriptional programs it regulates and the underlying molecular mechanisms are yet to be comprehensively understood. Here, we demonstrated that ESRRA serves as a central regulator in orchestrating the transcriptional activation of ERa-occupied super enhancers (ERSEs) and cognate ERa-target genes. Meanwhile, it downregulates the expression of cytosolic RNA sensors RIG1 and MDA5 to inhibit type I interferon (IFN) and type I IFN-stimulated genes (ISGs). In terms of mechanism, ESRRA is recruited to ERSEs together with ERain response to estrogen, and their binding with ESREs are regulated in a mutual-dependent manner. However, ESRRA directly binds to the promoter regions of RIG1 and MDA5 to suppress their expression. Consistent with these findings, pharmacological inhibition of ESRRA with its inverse agonist XCT790 inhibits estrogen/ERa-induced gene transcription, and enhances the type I IFN pathway and antitumor immunity to suppress breast cancer cell growth both in vitro and in vivo. Co-treatment with XCT790 and endocrine therapy drugs including ERa antagonist Tamoxifen or degrader Fulvestrant exhibited synergistic effects. Furthermore, combination treatment with XCT790 and tamoxifen re-sensitized Tamoxifen-resistant (TamR) ERa-positive breast cancer cells to Tamoxifen treatment. In summary, our findings unveiled that ESRRA is a pivotal regulator of ERSEs and estrogen/ERa-target gene activation, as well as the type I IFN signaling pathway, offering a promising therapeutic avenue for treating ERa-positive breast cancer in the clinic.

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