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Epigenomic profiling of enhancers identifies orphan nuclear receptors NR2F1 and NR2F2 as novel regulators of human neural crest

ABSTRACT: Epigenomic profiling of enhancers identifies orphan nuclear receptors NR2F1 and NR2F2 as novel regulators of human neural crest

PROVIDER: PRJNA140597 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR191352.fastq.gz	Fastqsanger.gz
	SRR191353.fastq.gz	Fastqsanger.gz
	SRR191354.fastq.gz	Fastqsanger.gz
	SRR191355.fastq.gz	Fastqsanger.gz
	SRR191356.fastq.gz	Fastqsanger.gz

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Epigenomic profiling of enhancers identifies orphan nuclear receptors NR2F1 and NR2F2 as novel regulators of human neural crest.

Project description:Combining an in vitro hNCC differentiation protocol with epigenomic profiling, we provide the first whole-genome characterization of cis-regulatory elements in this highly relevant cell type. With this data at hand, we have characterized the chromatin state and dynamics of all human gene promoters during the course of NCC in vitro differentiation. Most importantly, we have identified a large cohort of active and NCC-specific enhancers, which we showed to be functionally relevant in vivo, in the context of embryonic development. Finally, through sequence analysis of the identified NCC enhancers, we uncovered the orphan nuclear receptors NR2F1 and NR2F2 as novel hNCC transcriptional regulators both in vitro and in vivo. Genome-wide analysis of H3K27ac in chicken neural crest cells (NCC) obtained from stage 11-14 or stage 20 embryos

2012-09-13 | E-GEOD-38066 | biostudies-arrayexpress

Epigenomic profiling of enhancers identifies orphan nuclear receptors NR2F1 and NR2F2 as novel regulators of human neural crest.

2012-09-13 | GSE38066 | GEO

Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors

Project description:Nuclear receptors are iteratively deployed during neural crest development, from pre-induction through differentiation stages. NR2F1 and NR2F2 in particular have been proposed as broad regulators of early neural crest gene expression in mammals, but the timing, extent, and redundancy of their developmental requirement has remained unclear, as Nr2f1 and Nr2f2 single mouse mutants present only minimal craniofacial phenotypes. Here we report the dynamic expression patterns of Nr2f1 and Nr2f2 in the mouse cranial neural crest from specification through post-migratory stages. Combined conditional knockout of both Nr2f1 and Nr2f2 in the neural crest with Wnt1-Cre or Pax3Cre caused severe midfacial clefting, loss of the maxilla and palate, and hypoplasticity of all other facial skeletal elements except the distal mandible. These perinatal phenotypes were rooted in a major shortage of pharyngeal arch mesenchyme at mid-gestation. This in turn traced to a deficiency of migrating neural crest cells, first evident in the trailing part of the first arch migratory stream at embryonic day 8.75. RNAseq at a slightly earlier stage revealed downregulation of many migratory neural crest genes, including a possible direct target, the phospholipase Plcg2. These findings reveal a vital requirement for NR2F1/2 within the later-forming cranial neural crest.

2025-10-15 | GSE295092 | GEO

RNA-seq analysis of S16 Schwann cells treated with siRNA for Nr2f1/Nr2f2 (CoupTFI/CoupTFII)

Project description:In a previous study, we had compared SOX10-bound regulatory elements in Schwann cells and oligodendrocytes, and we identified a specific enrichment for nuclear receptor motifs at SOX10 binding sites in Schwann cells. We initially focused on NR2F1 and NR2F2 (CoupTF1/CoupTF2) since they are expressed from neural crest through Schwann cell maturity, and found that knockdown of nuclear receptors Nr2f1 and Nr2f2 in primary Schwann cells downregulated genes such as Myelin Basic Protein (Mbp) and Desert Hedgehog (Dhh). In this study, we have elucidated a NR2F-regulated target gene network in Schwann cells, which revealed enrichment for non-myelinating Schwann cell genes. Cut&Run assays in S16 Schwann cells revealed novel, genome-wide binding sites of NR2F1/2 and downstream transcription factors, Retinoid X Receptor (RXRG) and TEA-Domain factor (TEAD1).

2024-02-01 | GSE252428 | GEO

Genome-wide analysis of p300, H3K4me3, H3K4me1, H3K27me3 and H3K27ac in in vitro differentiated human neural crest cells (hNCC)

Project description:Combining an in vitro hNCC differentiation protocol with epigenomic profiling, we provide the first whole-genome characterization of cis-regulatory elements in this highly relevant cell type. With this data at hand, we have characterized the chromatin state and dynamics of all human gene promoters during the course of NCC in vitro differentiation. Most importantly, we have identified a large cohort of active and NCC-specific enhancers, which we showed to be functionally relevant in vivo, in the context of embryonic development. Finally, through sequence analysis of the identified NCC enhancers, we uncovered the orphan nuclear receptors NR2F1 and NR2F2 as novel hNCC transcriptional regulators both in vitro and in vivo. Genome-wide analysis of p300, H3K4me3, H3K4me1, H3K27me3, H3K27ac, NR2F1, NR2F2 and TFAP2A in in vitro differentiated human neural crest cells (hNCC)

2012-09-13 | E-GEOD-28874 | biostudies-arrayexpress

Epigenomic profiling of enhancers identifies orphan nuclear receptors NR2F1 and NR2F2 as novel regulators of human neural crest

Project description:This SuperSeries is composed of the following subset Series: GSE28874: Genome-wide analysis of p300, H3K4me3, H3K4me1, H3K27me3 and H3K27ac in in vitro differentiated human neural crest cells (hNCC) GSE28875: RNA-seq experiments in human neural crest cells (hNCC) Refer to individual Series

2012-09-13 | E-GEOD-28876 | biostudies-arrayexpress

RNA-seq experiments in human neural crest cells (hNCC)

Project description:Combining an in vitro hNCC differentiation protocol with epigenomic profiling, we provide the first whole-genome characterization of cis-regulatory elements in this highly relevant cell type. With this data at hand, we have characterized the chromatin state and dynamics of all human gene promoters during the course of NCC in vitro differentiation. Most importantly, we have identified a large cohort of active and NCC-specific enhancers, which we showed to be functionally relevant in vivo, in the context of embryonic development. Finally, through sequence analysis of the identified NCC enhancers, we uncovered the orphan nuclear receptors NR2F1 and NR2F2 as novel hNCC transcriptional regulators both in vitro and in vivo. RNA-seq experiments in human neural crest cells (hNCC)

2012-09-13 | E-GEOD-28875 | biostudies-arrayexpress

Schwann cell regulation by NR2F2 using Cut&Run

Project description:We focused on NR2F1 and NR2F2 (CoupTF1/CoupTF2) since they are expressed from neural crest through Schwann cell maturity, and found that knockdown of nuclear receptors Nr2f1 and Nr2f2 in primary Schwann cells downregulated genes such as Myelin Basic Protein (Mbp), Desert Hedgehog (Dhh), and N-Myc Downstream Regulated 1 (Ndrg1). In this study, we have elucidated a NR2F-regulated target gene network in Schwann cells, which revealed enrichment for non-myelinating Schwann cell genes. We used Cut&Run in S16 Schwann cells to show novel, genome-wide binding sites of NR2F1/2 and downstream transcription factors, YY1, SREBP1, Retinoid X Receptor (RXRG) and TEA-Domain factor (TEAD1). Our study elucidates the transcriptional cooperation that forms unique enhancer landscapes and the regulatory network that targets non-myelinating Schwann cells.

2024-01-01 | GSE247955 | GEO

RNA-seq experiments in human neural crest cells (hNCC)

2012-09-13 | GSE28875 | GEO

NR2C/F orphan receptors induce telomere-genome rearrangements in ALT

Project description:Most sarcomas have complex karyotype and are characterized by multiple chromosomal rearrangements. Moreover, sarcomas very frequently maintain their telomeres by recombination in the process called Alternative Lengthening of Telomeres (ALT) which enables their continuous growth and immortalization. Previously our group showed that orphan receptors bind specifically to the ALT telomeres and that their presence is important for the ALT mechanism. In these studies we focus on the function of orphan receptors at the telomeres and their contribution to telomeric recombination. We demonstrate that orphan receptors induce proximity of their binding sites in telomeric and genomic context and reveal novel aspects of ALT which are telomere-genome rearrangements which can underlie complexity of sarcomas. Our data perturb the dogma of telomere function in protecting the genome integrity. Here we show that in some cases telomeres may in fact drive genomic instability and chromosomal rearrangements by recombination with genomic sites. Characterization of TRF2 and orphan receptor NR2F/C2 binding sites in ALT (-) and ALT (+) cells.

2015-02-23 | E-GEOD-46237 | biostudies-arrayexpress

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