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Expression data from C2C12 myoblasts transduced with PRDM16 or vector

ABSTRACT: PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors. We used microarrays to detail the global programme of gene expression underlying the myoblasts-brown fat conversion induced by PRDM16. undifferentiated C2C12 myoblasts were stably expressed with retroviral PRDM16 or vector control. Total RNAs were isolated by Trizol, and subjected to Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Bruce Spiegelman

PROVIDER: E-GEOD-15895 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Initiation of myoblast to brown fat switch by a PRDM16-C/EBP-beta transcriptional complex.

Kajimura Shingo S Seale Patrick P Kubota Kazuishi K Lunsford Elaine E Frangioni John V JV Gygi Steven P SP Spiegelman Bruce M BM

Nature 20090729 7259

Brown adipose cells are specialized to dissipate chemical energy in the form of heat, as a physiological defence against cold and obesity. PRDM16 (PR domain containing 16) is a 140 kDa zinc finger protein that robustly induces brown fat determination and differentiation. Recent data suggests that brown fat cells arise in vivo from a Myf5-positive, myoblastic lineage by the action of PRDM16 (ref. 3); however, the molecular mechanisms responsible for this developmental switch is unclear. Here we s ...[more]

PMID: 19641492

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Expression data from C2C12 myoblasts transduced with PRDM16 or vector

Project description:PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors. We used microarrays to detail the global programme of gene expression underlying the myoblasts-brown fat conversion induced by PRDM16.

2009-07-31 | GSE15895 | GEO

PPARg agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein

Project description:Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPARγ ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here we show that PPARγ ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPARγ agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a novel therapeutic pathway for the treatment of obesity and diabetes. Microarray analysis of the differentiated inguinal adipocytes expressing sh-scr or sh-PRDM16 in the presence or absence of rosiglitazone (1uM). These samples were profiled using Affymetrix mouse 430A_2 arrays, representing 2 biological replicates for each samples (8 samples in total).

2012-03-06 | E-GEOD-35011 | biostudies-arrayexpress

Immortalized clonal brown, beige and white adipose cell lines

Project description:Brown fat generates heat via the mitochondrial uncoupling protein UCP1, defending against hypothermia and obesity. Recent data suggest that there are two distinct types of brown fat: classical brown fat derived from a myf-5 cellular lineage and UCP1-positive cells that emerge in white fat from a non-myf-5 lineage. Here, we report the isolation of “beige” cells from murine white fat depots. Microarray analysis of the differentiated clonal inguinal and interscapular adipocytes in the presence of forskolin (10mM). These samples were profiled using Affymetrix mouse 430 2.0 arrays, 26 samples in total.

2012-07-23 | E-GEOD-39562 | biostudies-arrayexpress

Cistromic and epigenomic changes in Prdm16 knock-out brown adipose tissue

Project description:Prdm16 is a transcription factor that drives a complete program of brown adipocyte differentiation, but the mechanism by which Prdm16 activates gene transcription remains unknown. Utilizing ChIP-seq teqhnique, we found that Prdm16 binds to chromatin at/near many brown fat-selective genes in BAT. Interestingly, Prdm16-deficiency dramatically reduced the binding of Med1 to Prdm16-target sites. Indeed, Prdm16 binds and recruits Med1 to BAT-enriched genes and the loss of Prdm16 caused a fundamental change in chromatin architecture at key BAT-selective genes and also reduced transcirptional activity. Moreover, Prdm16, through its interaction with Med1, defines and regulates the activity of super-enhancers that drive the expression of cell identity genes. Together, these data demonstrate that Prdm16 drives gene transcription by recruiting Med1 to control chromatin architecture and super-enhancers. Brown adipose tissues were collected from Prdm16 knockout and wiletype 9-month-old mice and ChIP-seq was performed for Prdm16, PolII, Med1, and H3K27ac.

2015-02-10 | E-GEOD-63965 | biostudies-arrayexpress

RNA-seq analysis in adipocytes that lack APPBP2 and/or PRDM16

Project description:We systematically determined the extent to which APPBP2 loss stimulate beige adipocyte biogenesis in a PRDM16-dependent fashion. To this end, we ran RNA-seq analysis in adipocytes that lack APPBP2 and/or PRDM16. By overlapping the transcriptome data with published dataset of brown/beige fat (Chondronikola et al., 2016; Perdikari et al., 2018; Shinoda et al., 2015a), we found that APPBP2 loss significantly increased 72 genes whose expression was enriched in brown adipocytes relative to white fat. Among 72 brown/beige fat-enriched genes, we found that 90.28% (65/72 genes) of them were regulated in a PRDM16-dependent manner. The data suggest that PRDM16 is required for the majority, if not all, of APPBP2’s action on brown fat genes

2022-06-06 | GSE196699 | GEO

PRDM16 represses the type I Interferon response in adipocytes [expression profiling]

Project description:PRDM16 is a strong activator of brown fat-specific genes, while also a repressor of white fat and muscle-specific genes. We asked what other pathways are regulated by PRDM16 in adipocytes that may be critical for brown and/or beige adipogenesis. Using microarray, we found PRDM16 also represses type I Interferon-stimulated genes (ISGs) in adipocytes.

2017-04-10 | GSE86016 | GEO

PPARg agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein

2012-03-06 | GSE35011 | GEO

Prdm16 Knockout Brown Adipose Tissue

Project description:Gene expression profile from brown adipose tissues of Prdm16 knockout and wile type mice. Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development. Brown adipose tissues were collected from Prdm16 knockout and wiletype mice with 4 biological replicates per condition. Experiment was done in two separate batch for 6-week-old and 11-month-old. Extracted RNA was hybridized to Agilent two-color arrays.

2014-04-09 | E-GEOD-55080 | biostudies-arrayexpress

Expression data from mouse primary brown preadipocytes

Project description:Brown adipocytes are specialized for heat generation and energy expenditure as a defense against cold and obesity. Recent studies demonstrate that brown adipocytes arise in vivo from a Myf5-positive, myoblastic progenitor by the action of PRDM16. Here, we identified a brown fat-enriched miRNA cluster mir-193b-365 as a key regulator of brown fat development. Blocking miR-193b and/or miR-365 in primary brown preadipocytes dramatically impaired brown adipocyte adipogenesis whereas myogenic markers were significantly induced. Forced expression of miR-193b and/or miR-365 in C2C12 myoblasts blocked the entire program of myogenesis, and miR-193b induced myoblasts to differentiate into brown adipocytes. Mir-193b-365 was upregulated by PRDM16. Our results demonstrate that mir-193b-365 serves as an essential regulator for brown fat differentiation, in part by repressing myogenesis.

2011-05-02 | GSE27614 | GEO

Prdm16 Knockout Brown Adipose Tissue

2014-04-09 | GSE55080 | GEO