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Genome-wide analysis of RXRa binding in mouse liver chromatin with ChIP-SEQ.

ABSTRACT: For the genome-wide analysis using ChIP-Seq on mouse liver cells, a full accounting of all RXRÎ± binding sites and of RXRa related gene regulations is expected to address the main knowledge gap around RXRÎ±.

ORGANISM(S): Mus musculus

PROVIDER: GSE21696 | GEO | 2014/04/01

SECONDARY ACCESSION(S): PRJNA125865

REPOSITORIES: GEO

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Genome-wide analysis of RXRa binding in mouse liver chromatin with ChIP-SEQ.

Project description:For the genome-wide analysis using ChIP-Seq on mouse liver cells, a full accounting of all RXRÎ± binding sites and of RXRa related gene regulations is expected to address the main knowledge gap around RXRÎ±. Liver tissue of wild type and hs-RXRa-del-exon4-/- mice, male and female for each genotype have been ChIP-Seq'ed for RXRa and Pol2.

2014-04-01 | E-GEOD-21696 | biostudies-arrayexpress

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Bladder-cancer-associated mutations in RXRA activate peroxisome proliferator-activated receptors to drive urothelial proliferation

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Project description:The cJun NH2-terminal kinase (JNK) signaling pathway in the liver promotes systemic changes in metabolism by regulating PPARa-dependent expression of the hepatokine FGF21. Hepatocyte-specific gene ablation studies demonstrated that the Mapk9 gene (encodes JNK2) plays a key mechanistic role. Mutually exclusive inclusion of exons 7a and 7b yields expression of the isoforms JNK2a and JNK2b. Here we demonstrate that Fgf21 gene expression and metabolic regulation is primarily regulated by the JNK2a isoform. To identify relevant substrates of JNK2a, we performed a quantitative phosphoproteomic study of livers isolated from control mice, mice with JNK-deficiency in hepatocytes, and mice that express only JNK2a or JNK2b in hepatocytes. We identified the JNK substrate RXRa as a protein that exhibited JNK2a-promoted phosphorylation in vivo. RXRa functions as a heterodimeric partner of PPARa and may therefore mediate the effects of JNK2a signaling on Fgf21 expression. To test this hypothesis, we established mice with hepatocyte-specific expression of wild-type or mutated RXRa proteins. We found that the RXRa phosphorylation site Ser260 was required for suppression of Fgf21 gene expression. Collectively, these data establish a JNK-mediated signaling pathway that regulates hepatic Fgf21 expression.

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