Regulation of adipocyte differentiation by IRF3
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ABSTRACT:
PROVIDER: PRJNA723554 | ENA |
REPOSITORIES: ENA
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Project description:The hypothesis tested is that IRF3 regulates adipogenesis and adipocyte function. Global gene expression of IRF3 wildtype (WT) and knockout (KO) adipocytes at different days during differentiation was compared. The results provide evidence on how IRF3 controls PPARg -regulated adipogenic program thereby regulate adipocyte differentiation.
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2022-02-18 | PXD024144 | Pride
Project description:Obesity-induced inflammation metabolic dysfunction, but the mechanisms remain elusive. Here we showed that the innate immune factor IRF3 is a direct transcriptional regulator of glucose homeostasis through induction of endogenous FAHFA hydrolase Aig1 in adipocytes. Adipocyte-specific knockout IRF3 protects mice against high-fat diet-induced insulin resistance, whereas overexpression of IRF3 in adipocytes promotes insulin resistance on a high-fat diet. Furthermore, pharmacological inhibition of AIG1 reversed obesity-induced insulin resistance and restored glucose homeostasis in the setting of adipocyte IRF3 overexpression. We therefore, identify the adipocyte IRF3/AIG1 axis as a crucial link between obesity-induced inflammation and insulin resistance and suggest an approach for limiting the metabolic dysfunction accompanying obesity.
2024-02-09 | GSE213048 | GEO
Project description:Adipocyte differentiation, also known as adipogenesis, is a crucial process for maintaining the adipocyte pool and plays a key role in insulin sensitivity and systemic metabolism. Adipogenesis is governed by master transcription factors, such as C/EBPβ. However, there remains an unmet need to identify novel transcriptional factors within the C/EBPβ regulatory network in the differentiation of primary human adipose-derived precursor cells (hAPCs). Chromatin immunoprecipitation and selective isolation of chromatin-associated proteins (ChIP-SICAP) and CRISPR/cas9 knockout (KO) screening approach was applied in hAPCs. RNA-seq and ChIP-seq were also utilized for pathway and gene enrichment analyses. We also constructed a APCs-specific KO mouse model. Deletion of CUX1 in hAPCs impairs adipogenesis, whereas CUX1 overexpression (OE) increases human adipogenesis. RNA-seq and ChIP-seq analyses reveal that CUX1 promotes the expression of key adipogenic genes, including PPARG, a master regulator of adipocyte fate determination. Interestingly, Cux1 deletion enhances, while CUX1-OE suppresses adipogenesis in mouse APCs (mAPCs). ChIP-seq analysis of CUX1 in mAPCs further supports its contrasting role in mice. Additionally, in vivo tracing of mAPCs shows that Cux1 deletion promotes adipocyte differentiation. Collectively, these findings highlight that CUX1 exerts species-specific regulation of adipogenesis, acting as a differential regulator of fat development in humans and mice.
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Project description:The diverse transcriptional mechanisms governing cellular differentiation and development of mammalian tissue remains poorly understood. Here we report that TAF7L, a paralogue of TFIID subunit TAF7, is enriched in adipocytes and mouse white fat tissue (WAT). Depletion of TAF7L reduced adipocyte-specific gene expression and compromised adipocyte differentiation as well as WAT development. Ectopic expression of TAF7L in myoblasts reprograms these muscle precursors into adipocytes upon induction. Genome-wide mRNA-seq expression profiling and ChIP-seq binding studies confirmed that TAF7L is required for activating adipocyte-specific genes via a dual mechanism wherein it interacts with PPARM-NM-3 at enhancers and TBP/Pol II at core promoters. In vitro binding studies confirmed that TAF7L forms complexes with both TBP and PPARM-NM-3. These findings suggest that TAF7L plays an integral role in adipocyte gene expression by targeting enhancers as a cofactor for PPARM-NM-3 and promoters as a component of the core transcriptional machinery. Genome-wide mapping of TAF7L and additional factors, and mRNA-seq expression profiling prior to and following mouse adipocyte differentiation.
2013-01-07 | E-GEOD-41937 | biostudies-arrayexpress
Project description:CUX1 Manifests Species-Dependent Regulation in Controlling Adipocyte Differentiation [ChIP-Seq]
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Project description:CUX1 Manifests Species-Dependent Regulation in Controlling Adipocyte Differentiation [RNA-Seq]
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