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Genome-wide analysis of JMJD1A and PPARγ binding in immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

ABSTRACT: Genome-wide analysis of JMJD1A and PPARγ binding in immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

PROVIDER: PRJNA421900 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6365586.fastq.gz	Fastqsanger.gz
	SRR6365587.fastq.gz	Fastqsanger.gz

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Genome-wide analysis of JMJD1A and PPARγ binding in immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

Project description:In acute cold stress in mammals, JMJD1A, an H3K9 demethylase, up-regulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals also have another mechanism to cope with long-term cold stress by inducing the browning of subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation independent acute Ucp1 induction in BAT and demethylation dependent chronic Ucp1 expression in beige-scWAT provide complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namlely β-adrenergic receptor and PPARγ activation, via PRDM16-PPARγ-P-JMJD1A complex for beige adipogenesis.

2018-02-16 | GSE107899 | GEO

RNA-sequence analysis of immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

2018-02-16 | GSE107900 | GEO

Genome-wide localization maps of JMJD1A, SWI/SNF components, and PPARγ in brown adipocytes treated with isoproterenol

Project description:We analyzed ChIP-seq profiles for H3K4me3, H3K27ac, BRG1, ARID1A, PPARγ and JMJD1A and FAIRE-seq open chromatin profile in immortalized brown adipocytes (iBATs) treated with 1 μM isporoterenol (ISO) or vehicle for 2 hr

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RNA-sequence analysis of immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

Project description:RNA-sequence analysis of immortalized, differentiated preadipocytes derived from inguinal subcutaneous white adipose tissue.

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Interaction between PPARγ and mTORC1 in the regulation of inguinal white adipose tissue transcriptome

Project description:Purpose: To investigate the involvement of mTORC1 as a mediator of the actions of the PPARγ ligand rosiglitazone in subcutaneous inguinal white adipose tissue transcriptome; Methods: Mice bearing regulatory associated protein of mTOR (Raptor) deletion and therefore mTORC1 deficiency exclusively in adipocytes (adiponectin Cre recombinase) and littermate controls were fed a high-fat diet supplemented or not with the PPARγ agonist rosiglitazone (30 mg/kg/day) for 8 weeks and evaluated for inguinal white adipose tissue transcriptome (Rnaseq); Results: 3,2425 genes had their correspondent mRNA levels altered by either adipocyte Raptor deficiency or rosiglitazone administration or their combination. Among those, 408 genes modulated by rosiglitazone required mTORC1. Conclusion: PPARγ and mTORC1 are essential partners in the regulation of a cluster of genes in inguinal white adipose tissue.

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Genome-wide analysis of JMJD1A binding in immortalized subcutaneous white adipose tissue cells.

Project description:Protein kinase A promotes beige adipogenesis downstream from β-adrenergic receptor signaling by phosphorylating proteins, including histone H3 lysine 9 (H3K9) demethylase JMJD1A. To ensure homeostasis, this process needs to be reversible however, this step is not well understood. We show that myosin phosphatase target subunit 1- protein phosphatase 1β (MYPT1-PP1β) phosphatase activity is inhibited via PKA-dependent phosphorylation, which increases phosphorylated JMJD1A and beige adipogenesis. Mechanistically, MYPT1-PP1β depletion resulted in JMJD1A-mediated H3K9 demethylation and activation of the Ucp1 enhancer/promoter regions. Interestingly, MYPT1-PP1β also dephosphorylates myosin light chain which regulates actomyosin tension-mediated activation of YAP/TAZ which directly stimulates Ucp1 gene expression. Preadipocyte specific Mypt1 deficiency increases cold tolerance with higher Ucp1 levels in subcutaneous white adipose tissues compared to control mice, confirming this regulatory mechanism in vivo. Thus, we have uncovered new regulatory cross-talk involved in beige adipogenesis that coordinates epigenetic regulation with direct activation of the mechano-sensitive YAP/TAZ transcriptional co-activators.

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Histone H3K9 Methyltransferase G9a Represses PPARγ Expression and Adipogenesis [Affymetrix expression data]

Project description:PPARγ promotes adipogenesis while Wnt proteins inhibit adipogenesis. However, the mechanisms that control expression of these positive and negative master regulators of adipogenesis remain incompletely understood. By genome-wide histone methylation profiling in preadipocytes, we find that among gene loci encoding adipogenesis regulators, histone methyltransferase (HMT) G9a-mediated repressive epigenetic mark H3K9me2 is enriched on the entire PPARγ locus. H3K9me2 and G9a levels decrease during adipogenesis, which correlates inversely with induction of PPARγ. Removal of H3K9me2 by G9a deletion enhances chromatin opening and binding of adipogenic transcription factor C/EBP-beta to PPARγ promoter, which promotes PPARγ expression. Interestingly, G9a represses PPARγ expression in an HMT activity-dependent manner but facilitates Wnt10a expression independent of its enzymatic activity. Consistently, deletion of G9a or inhibiting G9a HMT activity promotes adipogenesis. Finally, deletion of G9a in mouse adipose tissues increases adipogenic gene expression and tissue weight. Thus, by inhibiting PPARγ expression and facilitating Wnt10a expression, G9a represses adipogenesis. Examination of gene expression changes in G9a KO brown preadipocytes

2013-02-01 | E-GEOD-41456 | biostudies-arrayexpress

Human subcutaneous preadipocytes RNAseq

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Genome-Wide Profiling of Peroxisome Proliferator-Activated Receptor γ in Primary Epididymal, Inguinal, and Brown Adipocytes Reveals Depot-Selective Binding Correlated with Gene Expression

Project description:Here we have employed chromatin immunoprecipitation combined with deep sequencing to map and compare PPARγ binding in in vitro differentiated primary mouse adipocytes isolated from epididymal, inguinal, and brown adipose tissues. While these PPARγ binding profiles are overall similar, there are clear depot-selective binding sites. Most PPARγ binding sites previously mapped in 3T3-L1 adipocytes can also be detected in primary adipocytes, but there are a large number of PPARγ binding sites that are specific to the primary cells, and these tend to be located in closed chromatin regions in 3T3-L1 adipocytes. The depot-selective binding of PPARγ is associated with highly depot-specific gene expression. This indicates that PPARγ plays a role in the induction of genes characteristic of different adipocyte lineages and that preadipocytes from different depots are differentially preprogrammed to permit PPARγ lineage-specific recruitment even when differentiated in vitro.

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Dicer knockout mouse subcutaneous preadipocytes

Project description:Dicer is required for miRNA processing and RNA interference. Here we knocked out Dicer in SV40 T antigen immortalized subcutaneous preadipocytes isolated from Dicer flox mice by transducing these cells with adenoviruses harboring Cre recombinase. Control cells were transduced with adenovirus harboring GFP. We used microarrays to detail the gene expression profile of Dicer knockout preadipocytes.

2012-03-31 | GSE24683 | GEO

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