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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28876 | GEO | 2012/09/13

SECONDARY ACCESSION(S): PRJNA140597

REPOSITORIES: GEO

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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

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

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

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

| PRJNA140597 | ENA

Epigenomic annotation of enhancers predicts transcriptional regulators of human neural crest.

Project description:Neural crest cells (NCC) are a transient, embryonic cell population characterized by unusual migratory ability and developmental plasticity. To annotate and characterize cis-regulatory elements utilized by the human NCC, we coupled a hESC differentiation model with genome-wide profiling of histone modifications and of coactivator and transcription factor (TF) occupancy. Sequence analysis predicted major TFs binding at epigenomically annotated hNCC enhancers, including a master NC regulator, TFAP2A, and nuclear receptors NR2F1 and NR2F2. Although many TF binding events occur outside enhancers, sites coinciding with enhancer chromatin signatures show significantly higher sequence constraint, nucleosomal depletion, correlation with gene expression, and functional conservation in NCC isolated from chicken embryos. Simultaneous co-occupancy by TFAP2A and NR2F1/F2 is associated with permissive enhancer chromatin states, characterized by high levels of p300 and H3K27ac. Our results provide global insights into human NC chromatin landscapes and a rich resource for studies of craniofacial development and disease.

| S-EPMC3751405 | biostudies-literature

Regulation of the orphan nuclear receptor Nr2f2 by the DFNA15 deafness gene Pou4f3.

Project description:Hair cells are the mechanotransducing cells of the inner ear that are essential for hearing and balance. POU4F3--a POU-domain transcription factor selectively expressed by these cells--has been shown to be essential for hair cell differentiation and survival in mice and its mutation in humans underlies late-onset progressive hearing loss (DFNA15). The downstream targets of POU4F3 are required for hair cell differentiation and survival. We aimed to identify such targets in order to elucidate the molecular pathways involved in hair cell production and maintenance. The orphan thyroid nuclear receptor Nr2f2 was identified as a POU4F3 target using a subtractive hybridization strategy and EMSA analysis showed that POU4F3 binds to two sites in the Nr2f2 5' flanking region. These sites were shown to be required for POU4F3 activation as their mutation leads to a reduction in the response of an Nr2f2 5' flanking region reporter construct to POU4F3. Immunocytochemistry was carried out in the developing and adult inner ear in order to investigate the relevance of this interaction in hearing. NR2F2 expression in the postnatal mouse organ of Corti was shown to be detectable in all sensory epithelia examined and characterised. These data demonstrate that Nr2f2 is a direct target of POU4F3 in vitro and that this regulatory relationship may be relevant to hair cell development and survival.

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Study of Genetic Polymorphisms of Drug Transporters and Orphan Nuclear Receptors on Treatment Effects of Irinotecan

Project description:From 100 colorectal cancer patients being treated with FOLFIRI regimen or any kind of irinotecan containing regimen, blood samples for irinotecan and its metabolites levels and genotypes related with its metabolism will be collected. The association of their levels and genotypes and treatment effects will be evaluated.

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Orphan nuclear receptors as targets for drug development.

Project description:Orphan nuclear receptors regulate diverse biological processes. These important molecules are ligand-activated transcription factors that act as natural sensors for a wide range of steroid hormones and xenobiotic ligands. Because of their importance in regulating various novel signaling pathways, recent research has focused on identifying xenobiotics targeting these receptors for the treatment of multiple human diseases. In this review, we will highlight these receptors in several physiologic and pathophysiologic actions and demonstrate how their functions can be exploited for the successful development of newer drugs.

| S-EPMC3518931 | biostudies-literature

Human genetic variation within neural crest enhancers: molecular and phenotypic implications.

Project description:Developmental gene expression programmes are coordinated by the specialized distal cis-regulatory elements called enhancers, which integrate lineage- and signalling-dependent inputs to guide morphogenesis. In previous work, we characterized the genome-wide repertoire of active enhancers in human neural crest cells (hNCC), an embryonic cell population with critical roles in craniofacial development. We showed that in hNCC, co-occupancy of a master regulator TFAP2A with nuclear receptors NR2F1 and NR2F2 correlates with the presence of permissive enhancer chromatin states. Here, we take advantage of pre-existing human genetic variation to further explore potential cooperation between TFAP2A and NR2F1/F2. We demonstrate that isolated single nucleotide polymorphisms affecting NR2F1/F2-binding sites within hNCC enhancers can alter TFAP2A occupancy and overall chromatin features at the same enhancer allele. We propose that a similar strategy can be used to elucidate other cooperative relationships between transcription factors involved in developmental transitions. Using the neural crest and its major contribution to human craniofacial phenotypes as a paradigm, we discuss how genetic variation might modulate the molecular properties and activity of enhancers, and ultimately impact human phenotypic diversity.

| S-EPMC3682725 | biostudies-literature

Heterodimerization of TFAP2 pioneer factors drives epigenomic remodeling during neural crest specification.

Project description:Cell fate commitment involves the progressive restriction of developmental potential. Recent studies have shown that this process requires not only shifts in gene expression but also an extensive remodeling of the epigenomic landscape. To examine how chromatin states are reorganized during cellular specification in an in vivo system, we examined the function of pioneer factor TFAP2A at discrete stages of neural crest development. Our results show that TFAP2A activates distinct sets of genomic regions during induction of the neural plate border and specification of neural crest cells. Genomic occupancy analysis revealed that the repertoire of TFAP2A targets depends upon its dimerization with paralogous proteins TFAP2C and TFAP2B. During gastrula stages, TFAP2A/C heterodimers activate components of the neural plate border induction program. As neurulation begins, TFAP2A trades partners, and TFAP2A/B heterodimers reorganize the epigenomic landscape of progenitor cells to promote neural crest specification. We propose that this molecular switch acts to drive progressive cell commitment, remodeling the epigenomic landscape to define the presumptive neural crest. Our findings show how pioneer factors regulate distinct genomic targets in a stage-specific manner and highlight how paralogy can serve as an evolutionary strategy to diversify the function of the regulators that control embryonic development.

| S-EPMC6961570 | biostudies-literature

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