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Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function [ChIP-seq]

ABSTRACT: To identify transcription factors in Foxo1's network with H3K27ac ChIPseq performed in WT and beta cell-specific Foxo1 knockout beta cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE161026 | GEO | 2020/11/07

REPOSITORIES: GEO

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Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function [RNA-seq]

Project description:To investigate the relationship between key beta-cell transcription factors Hnf4a and Foxo1.

2020-11-07 | GSE161027 | GEO

Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function

Project description:Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function

| PRJNA675131 | ENA

Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-07 | GSE161028 | GEO

Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function [ChIP-seq]

Project description:Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function [ChIP-seq]

| PRJNA675132 | ENA

Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function [RNA-seq]

Project description:Antagonistic role of Hnf4a and FoxO1 metabolic networks through enhancer interactions in beta-cell function [RNA-seq]

| PRJNA675133 | ENA

Antagonistic epistasis of Hnf4α and FoxO1 metabolic networks through enhancer interactions in β-cell function.

Project description:ObjectiveGenetic and acquired abnormalities contribute to pancreatic β-cell failure in diabetes. Transcription factors Hnf4α (MODY1) and FoxO1 are respective examples of these two components and act through β-cell-specific enhancers. However, their relationship is unclear.MethodsIn this report, we show by genome-wide interrogation of chromatin modifications that ablation of FoxO1 in mature β-cells enriches active Hnf4α enhancers according to a HOMER analysis.ResultsTo model the functional significance of this predicted unusual enhancer utilization, we generated single and compound knockouts of FoxO1 and Hnf4α in β-cells. Single knockout of either gene impaired insulin secretion in mechanistically distinct fashions as indicated by their responses to sulfonylurea and calcium fluxes. Surprisingly, the defective β-cell secretory function of either single mutant in hyperglycemic clamps and isolated islets treated with various secretagogues was completely reversed in double mutants lacking FoxO1 and Hnf4α. Gene expression analyses revealed distinct epistatic modalities by which the two transcription factors regulate networks associated with reversal of β-cell dysfunction. An antagonistic network regulating glycolysis, including β-cell "disallowed" genes, and a synergistic network regulating protocadherins emerged as likely mediators of the functional restoration of insulin secretion.ConclusionsThe findings provide evidence of antagonistic epistasis as a model of gene/environment interactions in the pathogenesis of β-cell dysfunction.

| S-EPMC8225970 | biostudies-literature

Effect of osteoblast-specific constitutive activation of beta-catenin or deletion of FoxO1 on gene expression in mice

Project description:The gene expression of mice with osteoblast-specific beta-catenin activation or FoxO1 deactivation are each compared to that of Wt. A. Wt mice (n=4) B. Osteoblast specific beta-catenin constitutively expressed mice (n=3) C. Osteoblast specific FoxO1 deleted mice (n=3)

2014-01-21 | E-GEOD-43242 | biostudies-arrayexpress

TDAG51 is a novel coactivator of FoxO1

Project description:Tight regulation of Toll-like receptor (TLR)-mediated inflammatory responses is important in innate immunity. Here, we show that T cell death-associated gene 51 (TDAG51/PHLDA1) is a novel coactivator of the transcription factor FoxO1, regulating inflammatory mediator production in the lipopolysaccharide (LPS)-induced inflammatory response. TDAG51 induction by LPS stimulation was mediated by the TLR2/4 signaling pathway in bone marrow-derived macrophages (BMMs). LPS-induced inflammatory mediator production was significantly decreased in TDAG51-deficient BMMs. In TDAG51-deficient mice, LPS- or pathogenic Escherichia coli infection-induced lethal shock was reduced by decreasing serum proinflammatory cytokine levels. The recruitment of 14-3-3 to FoxO1 was competitively inhibited by the TDAG51-FoxO1 interaction, leading to blockade of FoxO1 cytoplasmic translocation and thereby strengthening FoxO1 nuclear accumulation. TDAG51/FoxO1 double-deficient BMMs showed significantly reduced inflammatory mediator production compared with TDAG51- or FoxO1-deficient BMMs. TDAG51/FoxO1 double deficiency protected mice against LPS- or pathogenic E. coli infection-induced lethal shock by weakening the systemic inflammatory response. Thus, these results indicate that TDAG51 acts as a coactivator of the transcription factor FoxO1, leading to strengthened FoxO1 activity in the LPS-induced inflammatory response.

2023-06-24 | PXD039815 | Pride

Mst1-mediated phosphorylation of FoxO1 and C/EBP-β Stimulates Cell-protective Mechanisms in Cardiomyocytes

Project description:The molecular mechanisms by which FoxO transcription factors mediate diametrically opposite cellular responses, namely death and survival, remain unknown. Mst1 phosphorylates FoxO1 Ser209/Ser215/Ser218/Thr228/Ser232/Ser243, thereby inducing nuclear translocation of FoxO1 in cardiomyocytes. Mst1 inhibits the FoxO1-mediated transcription of proapoptotic genes but promotes that of prosurvival genes. Mst1 increases FoxO1-C/EBP-β interaction and phosphorylates C/EBP-β at Thr299, thereby promoting transcription of prosurvival genes. Myocardial ischemia/reperfusion (I/R) injury was larger in cardiac-specific FoxO1 knockout (c-FoxO1–/–) mice than in control mice. However, the concurrent presence of C/EBP-β T299E phospho-mimetic mutation reduced infarct size in c-FoxO–/– mice. The C/EBP-β phospho-mimetic mutant exhibited a higher binding to the promoter of prosurvival genes compared to wild-type C/EBP-β. In conclusion, phosphorylation of FoxO1 by Mst1 inhibits the binding of FoxO1 to pro-apoptotic gene promoters but enhances its binding to C/EBP-β, phosphorylation of C/EBP-β, and transcription of prosurvival genes, which stimulate protective mechanisms in the heart.

2022-09-12 | GSE213010 | GEO

BioID HEK293T PAX3-FOXO1 proximity labelling

Project description:PAX3-FOXO1 is a fusion transcription factor that is the main driver of tumorigenesis leading to the development of alveolar rhabdomyosarcoma (aRMS). Since aRMS cells are addicted to PAX3-FOXO1 activity, the fusion protein also represents a major target for therapeutic interference, which is however challenging as transcription factors usually cannot be inhibited directly by small molecules. Hence, characterization of the biology of PAX3-FOXO1 might lead to the discovery of new possibilities for an indirect inhibition of its activity. Here, our goal was to characterize the proteomic neighborhood of PAX3-FOXO1 and to find candidates potentially affecting its activity and tumor cell viability. Towards this aim, we expressed BirA fused versions of PAX3-FOXO1 (N- and C-terminal) in HEK293T cells under presence of biotin. In the control setup, we expressed the BirA enzyme alone. After Streptavidin purification of biotinylated proteins, we performed mass spectrometry and quantified relative abundances compared to control conditions. This enabled us to determine PAX3-FOXO1 proximal proteins, which we investigated further in orthogonal endogenous systems.

2021-09-16 | PXD022187 | Pride

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