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Atrial Identity Is Determined by A COUP-TFII Regulatory Network (ChIP-Seq)

ABSTRACT: Embryonic cardiomyocytes possess the plasticity to choose between atrial and ventricular fates. For a limited window of time, the transcription factor COUP-TFII (Nr2f2) sufficiently and essentially confers the atrial identity through direct and indirect regulation of nearly half of chamber specific genes. Examination of COUP-TFII binding sites in embryonic artia

ORGANISM(S): Mus musculus

SUBMITTER: San-pin Wu

PROVIDER: E-GEOD-46497 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Atrial identity is determined by a COUP-TFII regulatory network.

Wu San-pin SP Cheng Chiang-Min CM Lanz Rainer B RB Wang Tiannan T Respress Jonathan L JL Ather Sameer S Chen Wen W Tsai Shaw-Jenq SJ Wehrens Xander H T XH Tsai Ming-Jer MJ Tsai Sophia Y SY

Developmental cell 20130501 4

Atria and ventricles exhibit distinct molecular profiles that produce structural and functional differences between the two cardiac compartments. However, the factors that determine these differences remain largely undefined. Cardiomyocyte-specific COUP-TFII ablation produces ventricularized atria that exhibit ventricle-like action potentials, increased cardiomyocyte size, and development of extensive T tubules. Changes in atrial characteristics are accompanied by alterations of 2,584 genes, of ...[more]

PMID: 23725765

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Genome-wide Profiling of NR2F2 (COUP-TFII) Binding in Human Endometrial Stromal Cells [ChIP-Seq]

Project description:ChickenM-BM- ovalbumin upstream promoter-transcription factor II (COUP-TFII; NR2F2) is an orphan nuclear receptor involved in cell-fate specification, organogenesis, angiogenesis and metabolism. Ablation of COUP-TFII in the mouse uterus causes infertility due to defects in embryo attachment and impaired uterine stromal cell decidualization. Although the function of COUP-TFII in uterine decidualization has been described in mice, its role in the human uterus remains unknown. To better elucidate the mechanisms with which COUP-TFII regulates target gene transcription, genome-wide COUP-TFII binding sites in human endometrial stromal cells (HESC) treated with deciduogenic hormones were identified using ChIP-seq. A total of 16,298 intervals (binding regions) for COUP-TFII were identified compared with the input in HESC chromatin with a very low false discovery rate (0.17%) using a stringent cutoff of p =1x10-10. Distribution of intervals showed that more than half (58.6%) of the COUP-TFII binding sites are located within 10 kb of gene boundaries. 7.5% of total intervals reside within the 10 kb promoter region. A total of 6,077 unique genes were identified to have COUP-TFII binding sites within 10 kb of their gene boundaries. Examination of NR2F2 binding in pooled primary human endometrial stromal cells from 6 healthy women upon decidualization with a hormone cocktail of cAMP, E2 and medroxyprogesterone acetate.

2013-11-02 | E-GEOD-52008 | biostudies-arrayexpress

A COUP-TFII human embryonic stem cell reporter line to identify and purify atrial cardiomyocytes

Project description:Here, we targeted mCherry to the COUP-TFII genomic locus in NKX2.5eGFP/+ hPSCs. Upon differentiation to atrial and ventricular cardiomyocytes (CMs) this dual atrial COUP-TFIImCherry/+-NKX2.5eGFP/+ reporter line allowed identification and selection of GFP+ (G+)/mCherry+ (M+) CMs following cardiac differentiation. These cells exhibited transcriptional and functional properties of atrial CMs, whereas G+/M- CMs displayed ventricular characteristics. Via CRISPR/Cas9-mediated knockout, we demonstrated that COUP-TFII is not required atrial specification in hPSCs.

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Orphan nuclear receptor COUP-TFII enhances myofibroblasts glycolysis leading to kidney fibrosis

Project description:Recent studies demonstrated that metabolic disturbance, such as augmented glycolysis, contributes to fibrosis. The molecular regulation of this metabolic perturbation in fibrosis, however, has been elusive. COUP-TFII (also known as NR2F2) is an important regulator of glucose and lipid metabolism. Its contribution to organ fibrosis is undefined. Here, we found increased COUP-TFII expression in myofibroblasts in human fibrotic kidneys, lungs, kidney organoids, and mouse kidneys after injury. Genetic ablation of COUP-TFII in mice resulted in attenuation of injury-induced kidney fibrosis. A non-biased proteomic study revealed the suppression of fatty acid oxidation and the enhancement of glycolysis pathways in COUP-TFII overexpressing fibroblasts. Overexpression of COUP-TFII in fibroblasts induced augmented glycolysis and production of alpha smooth muscle actin (αSMA) and collagen1. Knockout of COUP-TFII decreased glycolysis and collagen1 levels in fibroblasts. Chip-qPCR revealed the binding of COUP-TFII on the promoter of PGC1α. Overexpression of COUP-TFII reduced the cellular level of PGC1α. Targeting COUP-TFII serves as a novel treatment approach for mitigating fibrosis in chronic kidney disease and potentially fibrosis in other organs.

2021-04-27 | PXD024035 | Pride

Identification of a Facial Enhancer

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Atrial Identity Is Determined by A COUP-TFII Regulatory Network (ChIP-Seq)

Project description:Embryonic cardiomyocytes possess the plasticity to choose between atrial and ventricular fates. For a limited window of time, the transcription factor COUP-TFII (Nr2f2) sufficiently and essentially confers the atrial identity through direct and indirect regulation of nearly half of chamber specific genes.

2013-06-07 | GSE46497 | GEO

Transcriptional regulation patterns revealed by high-resolution chromatin immunoprecipitation during cardiac hypertrophy

Project description:Purpose: To identify the differential transcriptional patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Results: Our data revealed novel transcriptional patterns during cardiac growth conditions. The results showed that most of the essential genes are regulated by promoter clearance of paused RNA pol II, while de novo recruitment is required for regulation of mostly speclaized genes during cardiac growth. We have identified two major modes of gene regulation durign cardiac hypertrophy and four transcriptional growth patterns. The results are published in January 2013 issue of Journal of Biological Chemistry. Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for RNA polII and H3K9ac- ChIP-Seq.

2013-09-06 | E-GEOD-50637 | biostudies-arrayexpress

Expression data from control and COUP-TFII siRNA treated PC3 cells

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2011-10-25 | GSE33182 | GEO

Expression data from control and COUP-TFII siRNA treated HUVEC cells

Project description:COUP-TFII plays a critical role in angiogenesis during development. It has also been shown to suppress Notch signaling pathway to confer vein identity. However, the downstream targets and the mechanism mediate COUP-TFII function to regulate these processes remain elusive. To identify the downstream targets and the mechanism by which COUP-TFII regulates agiogenesis and vein specification, we knocked down COUP-TFII in HUVEC cells using COUP-TFII specific siRNA and used microarray analysis to identify downstream targets. Interestingly, we found the expression of many genes in the cell cycle pathway and Notch signaling pathway are significantly altered in the COUP-TFII depleted cells.

2011-10-28 | GSE33301 | GEO

Expression profile of COUP-TFII overexpressing mouse ventral midbrain

Project description:Elevated COUP-TFII levels are found in Parkinson’s disease. COUP-TFII overexpression in mouse dopaminergic neurons caused neurodegeneration. The goal of this study is to identify molecular mechanisms of COUP-TFII-mediated cell death through RNAseq.

2020-05-29 | GSE132874 | GEO

Genome wide TFIIB binding during postnatal and pressure-induced cardiac hypertrophy

Project description:Purpose: To identify the differential TFIIB bindingl patterns during postnatal cardiac growth, pressure-induced cardiac hypertrophy and adult mouse hearts Methods: Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq. Results: In accordance with previosly published data (Sayed D, et. al. JBC, 2013 Jan 25;288(4):2546-58) with genome wide polII and H3K9ac status during cardiac hypertrophy (GSE50637), Denovo TFIIB recruitment was restricted to speclaized genes with cardiac hypertrophy. Hearts were extracted from 1-2day old C57 mice, from mice subjecetd to Transaortic coarctation or adult mice. The hearts were sent to Active Motif for TFIIB- ChIP-Seq.

2014-11-17 | E-GEOD-56813 | biostudies-arrayexpress

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