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Genome-wide binding profiles of nuclear FGFR1, RXRα and Nur77 in pluripotent mouse Embryonic Stem Cells and during Retinoic Acid-induced differentiation

ABSTRACT: We report the genome-wide binding patterns of nuclear FGFR1, RXRα and Nur77 in pluripotenet mESC and as mESC differentiate towared a neuronal lineage in response to high levels of Retinoic Acid treatment in vitro. We also report the genome-wide incorporation of histone varant H3.3 into chromatin specifically during Retinoic Acid-induced differentiation. This study presents nuclear FGFR1 as a global factor that controls genomic function by binding within the promoters of thousands of genes, both alone and in cooperation with RXR, Nur77 and histone H3.3, by targeting consensus DNA sequences of diverse transcription factor families. As such, it identifies a previously unknown, multifaceted form of control of major ontogenic pathways and gene networks targeted by the nuclear form of FGFR1.

ORGANISM(S): Mus musculus

PROVIDER: GSE65695 | GEO | 2015/05/01

SECONDARY ACCESSION(S): PRJNA274739

REPOSITORIES: GEO

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Genome-wide binding profiles of nuclear FGFR1, RXR? and Nur77 in pluripotent mouse Embryonic Stem Cells and during Retinoic Acid-induced differentiation

Project description:We report the genome-wide binding patterns of nuclear FGFR1, RXR? and Nur77 in pluripotenet mESC and as mESC differentiate towared a neuronal lineage in response to high levels of Retinoic Acid treatment in vitro. We also report the genome-wide incorporation of histone varant H3.3 into chromatin specifically during Retinoic Acid-induced differentiation. This study presents nuclear FGFR1 as a global factor that controls genomic function by binding within the promoters of thousands of genes, both alone and in cooperation with RXR, Nur77 and histone H3.3, by targeting consensus DNA sequences of diverse transcription factor families. As such, it identifies a previously unknown, multifaceted form of control of major ontogenic pathways and gene networks targeted by the nuclear form of FGFR1. Examination of nuclear FGFR1, RXR?, and Nur77 binding sites in 2 celluar states. Examination of H3.3 incorporation in 1 cellular state.

2015-05-01 | E-GEOD-65695 | biostudies-arrayexpress

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Project description:Genome-wide binding profiles of nuclear FGFR1, RXRα and Nur77 in pluripotent mouse Embryonic Stem Cells and during Retinoic Acid-induced differentiation

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Nuclear receptor Nur77 and Yin-Yang 1 synergistically increase mitochondrial abundance and activity in macrophages [ChIP-seq]

Project description:Mitochondrial biogenesis requires precise regulation of both mitochondrial-encoded and nuclear-encoded genes. Nuclear receptor Nur77 is known to regulate mitochondrial metabolism in macrophages and skeletal muscle cells. Here, we compared genome-wide Nur77 binding site and target gene expression in these two cell types, which revealed conserved roles for this nuclear receptor in the regulation of nuclear-encoded mitochondrial ribosomal proteins (MRP) and enrichment of motifs for the transcription factor Yin-Yang 1 (YY1). We show that Nur77 and YY1 interact, that YY1 increases Nur77 activity, and that their binding sites are co-enriched at MRP gene loci. Nur77 and YY1 co-expression synergistically increases mitochondrial abundance and activity in macrophages but not skeletal muscle. As such, we identify a macrophage-specific Nur77-YY1 interaction that enhances mitochondrial metabolism.

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Nuclear receptor Nur77 and Yin-Yang 1 synergistically increase mitochondrial abundance and activity in macrophages [RNA-seq]

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Project description:Our project focuses on retinoic acid (RA) effect on hepatic lipid homeostasis. Even though RA has more than one receptor including retinoids x receptor (RXR) and retinoic acid receptor (RAR), most probably, RA effect on lipid homeostasis is mediated by RXR and its partners such as PXR, FXR, and PPAR. So we treated the wild type and RXRα-knockout mice by retinoic acid to check the global gene expression especially for lipid homeostasis genes. We used microarrays to observe the global gene expression underlying hepatic lipid homeostasis.

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