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Expression data from mouse primary brown preadipocytes

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE27614 | GEO | 2011/05/02

SECONDARY ACCESSION(S): PRJNA138265

REPOSITORIES: GEO

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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. To study if miR-193b-365 is required for brown adipocyte adipogenesis, mRNAs from cultured primary brown adipocytes (Day 4) transfected with each locked nucleic acid (LNA) miRNA inhibitor or Control inhibitor were analyzed by microarray analysis.

2011-05-02 | E-GEOD-27614 | biostudies-arrayexpress

Expression data from C2C12 myoblasts transduced with PRDM16 or vector

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Expression data from C2C12 myoblasts transduced with PRDM16 or vector

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Project description:Brown adipose (BAT) development and function are unaffected by the absence of miR-193b/365-1

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In vivo development, differentiation and function of brown fat proceeds in the absence of miRNAs 193b and 365-1

Project description:Brown adipose (BAT) development and function are unaffected by the absence of miR-193b/365-1 We refer to wild-type mice (+/+) as WT and to mice lacking the mir-193b (-/-) as Null mice.

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

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Epigenome in brown and white adipose tissue

Project description:PR (PRD1-BF1-RIZ1 homologous) domain-containing 16 (PRDM16) drives a brown fat differentiation program, but the mechanisms by which PRDM16 activates brown fat-selective genes have been unclear. Through chromatin immunoprecipitation (ChIP) followed by deep sequencing (ChIP-seq) analyses in brown adipose tissue (BAT), we reveal that PRDM16 binding is highly enriched at a broad set of brown fat-selective genes. Importantly, we found that PRDM16 physically binds to MED1, a component of the Mediator complex, and recruits it to superenhancers at brown fat-selective genes. PRDM16 deficiency in BAT reduces MED1 binding at PRDM16 target sites and causes a fundamental change in chromatin architecture at key brown fat-selective genes. Together, these data indicate that PRDM16 controls chromatin architecture and superenhancer activity in BAT.

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