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The role of the bHLH factor E47 in modulating hepatic glucocorticoid receptor action (metabolism) [RNA-seq]

ABSTRACT: We performed RNA sequencing in different wildtype and E47ko tissues in response to treatment with glucocorticoids. We show a global deregulation of gene expression programs involved in lipid, triglyceride and cholesterol metabolism & transport for E47 mutant liver tissue.

ORGANISM(S): Mus musculus

PROVIDER: GSE111877 | GEO | 2018/11/30

REPOSITORIES: GEO

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The role of the bHLH factor E47 in modulating hepatic glucocorticoid receptor action (metabolism) [ChIP-seq]

Project description:We performed ChIP-Sequencing for E2A and GR in mouse livers and demonstrate that E47 co-occupies metabolic promoters and enhancers together with GR. Together with the corresponding RNA-Seq data, our results illustrate how GR and E47 synergize during the transcriptional activation of hepatic metabolism.

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The role of the bHLH factor E47 in modulating hepatic glucocorticoid receptor action (metabolism) [RNA-seq]

Project description:The role of the bHLH factor E47 in modulating hepatic glucocorticoid receptor action (metabolism) [RNA-seq]

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The role of the bHLH factor E47 in modulating hepatic glucocorticoid receptor action (metabolism) [ChIP-seq]

Project description:The role of the bHLH factor E47 in modulating hepatic glucocorticoid receptor action (metabolism) [ChIP-seq]

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E47 modulates hepatic glucocorticoid action.

Project description:Glucocorticoids (GCs) are effective drugs, but their clinical use is compromised by severe side effects including hyperglycemia, hyperlipidemia and obesity. They bind to the Glucocorticoid Receptor (GR), which acts as a transcription factor. The activation of metabolic genes by GR is thought to underlie these adverse effects. We identify the bHLH factor E47 as a modulator of GR target genes. Using mouse genetics, we find that E47 is required for the regulation of hepatic glucose and lipid metabolism by GR, and that loss of E47 prevents the development of hyperglycemia and hepatic steatosis in response to GCs. Here we show that E47 and GR co-occupy metabolic promoters and enhancers. E47 is needed for the efficient recruitment of GR and coregulators such as Mediator to chromatin. Altogether, our results illustrate how GR and E47 regulate hepatic metabolism, and might provide an entry point for novel therapies with reduced side effects.

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Gene expression analysis of PANC-1 cells inducibly expressing the bHLH protein E47

Project description:Analysis of induced E47 expression on PDA cells at the gene expression level.The hypothesis tested in the present study was that PDA cells can be reprogrammed to revert to their original quiescent acinar cell phenotype by stimulating a tamoxifen inducible form of E47 fused to a modified estrogen (E47-ER) receptor . Results provide important information on the remarkable ability of E47ER to trigger reactivation of the acinar cell differentiation program and cell cycle arrest in PDA cells.

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ChIP-MS for GR in liver from wild type and E47 mutant mice

Project description:Glucocorticoids (GCs) are widely prescribed effective drugs, but their clinical use is compromised by severe side effects including hyperglycemia, hyperlipidemia and obesity. They bind to the Glucocorticoid Receptor (GR), which acts as a ligand-gated transcription factor. The transcriptional activation of metabolic genes by GR is thought to underlie these undesired adverse effects. Using mouse genetics, ChIP-Seq, RNA-Seq and ChIP-MS, we found that the bHLH transcription factor E47 is required for the regulation of hepatic glucose and lipid metabolism by GR in vivo, and that loss of E47 prevents the development of hyperglycemia and hepatic steatosis in response to GCs. Here we show that E47 and GR co-occupy metabolic promoters and enhancers. E47 is needed for the efficient binding of GR to chromatin and for the adequate recruitment of coregulators such as Mediator. Taken together, our results illustrate how GR and E47 regulate hepatic metabolism, and how inhibition of E47 might provide an entry point for novel GC therapies with reduced side effect profiles. These ChIP-MS data sets show IPs for GR in both wildtype and E47 mutant mouse livers treated with the synthetic glucocorticoid Dexamethasone.

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Identification of E47 targets

Project description:In maturing T-lineage cells, the helix-loop-helix protein E47 has been shown to enforce a critical proliferation and developmental checkpoint commonly referred to as Î² selection. To examine how E47 regulates cellular expansion and developmental progression, we have used an E2A deficient lymphoma cell line and DNA microarray analysis to identify immediate E47 target genes. Hierarchical cluster analysis of gene expression patterns revealed that E47 coordinately regulates the expression of genes involved in cell survival, cell growth, lipid metabolism, stress response and lymphoid maturation. These include Cdk6, CD25, Tox, Gadd45a, Gadd45b, Gfi1, Gfi1b, Socs1, Socs3, Id2, Eto2 and Xbp1. We propose a regulatory network linking JAK/STAT mediated signaling, E47 and SOCS proteins in a common pathway. Finally, we suggest that the aberrant activation of Cdk6 in E47 deficient T-lineage cells contributes to the development of lymphoid malignancy. We used the 1F9 cell line, originally isolated from E2A deficient thymomas. To identify E47 target genes, 1F9 cells were transduced with a retrovirus carrying an E47/estrogen receptor (E47ER) hybrid protein. Control cells were transduced with virus carrying the bHLH region but lacking the N-terminal transactivation domain. Both retroviral constructs also directed the expression of human CD25 (hCD25) to allow rapid isolation of transduced cells. One day post-infection, cells were incubated with 4-hydroxytamoxifen (4-OHT) for a period of six hours, to activate the E47ER fusion protein. hCD25 positive cells were purified using magnetic beads, RNA was isolated and used to generate probes for hybridization to murine oligonucleotide microarrays.

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Project description:To find the target genes regulated by E47 in hematopoietic progenitor cells Keywords: genetic modification

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Expression data of in vitro generated regulatory T cells overexpressing E47

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