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Jmjd3-mediated H3K27me3 dynamics orchestrate brown fat cell fate transition and regulate white fat plasticity (RNA-Seq)

ABSTRACT: We performed RNA-Seq for brwon fat, epididymal white fat and soleus muscle of mice to identify brown fat-selective, white fat-selective and common fat genes. RNA-Seq for brown fat, white fat and soleus muscle of wild type C56BL6 mice.

ORGANISM(S): Mus musculus

SUBMITTER: Yongxu Wang

PROVIDER: E-GEOD-56367 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Jmjd3-Mediated H3K27me3 Dynamics Orchestrate Brown Fat Development and Regulate White Fat Plasticity.

Pan Dongning D Huang Lei L Zhu Lihua J LJ Zou Tie T Ou Jianhong J Zhou William W Wang Yong-Xu YX

Developmental cell 20151125 5

Progression from brown preadipocytes to adipocytes engages two transcriptional programs: the expression of adipogenic genes common to both brown fat (BAT) and white fat (WAT), and the expression of BAT-selective genes. However, the dynamics of chromatin states and epigenetic enzymes involved remain poorly understood. Here we show that BAT development is selectively marked and guided by repressive H3K27me3 and is executed by its demethylase Jmjd3. We find that a significant subset of BAT-selectiv ...[more]

PMID: 26625958

Similar Datasets

Jmjd3-mediated H3K27me3 dynamics orchestrate brown fat cell fate transition and regulate white fat plasticity (RNA-Seq)

Project description:We performed RNA-Seq for brwon fat, epididymal white fat and soleus muscle of mice to identify brown fat-selective, white fat-selective and common fat genes.

2015-12-31 | GSE56367 | GEO

Jmjd3-mediated H3K27me3 dynamics orchestrate brown fat cell fate transition and regulate white fat plasticity

Project description:We performed ChIP-seq to chart genome-wide maps of H3K27me3 in brown preadipocytes and mature brown adipocytes. We observed a subset of brown fat-specific genes, but not common fat genes or white fat-specific genes, possess the H3K27me3 mark in preadipocytes, and this mark is erased in mature adipocytes. H3K27me3 ChIP-seq in brown preadipocytes and mature adipocytes.

2015-12-31 | E-GEOD-55469 | biostudies-arrayexpress

Jmjd3-mediated H3K27me3 dynamics orchestrate brown fat cell fate transition and regulate white fat plasticity

2015-12-31 | GSE55469 | GEO

RNAseq of murine brown fat, white fat and skeletal muscle

Project description:Used to control identified tissue type, the brown fat, white fat and skeletal muscle were dissected from mice (N=3) at room temperature (23C)

2018-09-18 | E-MTAB-7175 | biostudies-arrayexpress

Jmjd3-Mediated H3K27me3 Dynamics Orchestrate Brown Fat Development and Regulate White Fat Plasticity.

Project description:Progression from brown preadipocytes to adipocytes engages two transcriptional programs: the expression of adipogenic genes common to both brown fat (BAT) and white fat (WAT), and the expression of BAT-selective genes. However, the dynamics of chromatin states and epigenetic enzymes involved remain poorly understood. Here we show that BAT development is selectively marked and guided by repressive H3K27me3 and is executed by its demethylase Jmjd3. We find that a significant subset of BAT-selective genes, but not common fat genes or WAT-selective genes, are demarcated by H3K27me3 in both brown and white preadipocytes. Jmjd3-catalyzed removal of H3K27me3, in part through Rreb1-mediated recruitment, is required for expression of BAT-selective genes and for development of beige adipocytes both in vitro and in vivo. Moreover, gain- and loss-of-function Jmjd3 transgenic mice show age-dependent body weight reduction and cold intolerance, respectively. Together, we identify an epigenetic mechanism governing BAT fate determination and WAT plasticity.

| S-EPMC4679478 | biostudies-literature

RNAseq of murine brown fat, white fat and skeletal muscle

Project description:RNAseq of murine brown fat, white fat and skeletal muscle

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Loss of the tumor suppressor gene AIP mediates the browning of human brown fat tumors

Project description:Human brown fat tumors (hibernomas) display concomitant loss of the tumor suppressor genes MEN1 and AIP. In the present study, we hypothesized that the brown fat phenotype is attributed to these mutations. Accordingly, we demonstrate that silencing of AIP in human brown preadipocytic and white fat cell lines results in the induction of the brown fat marker UCP1. In human adipocytic tumors, loss of MEN1 was found both in white (one out of 51 lipomas) and brown fat tumors. In contrast, concurrent loss of AIP was always accompanied by a brown fat morphology. We conclude that this white-to-brown phenotype switch in brown fat tumors is mediated by the loss of AIP.

2017-08-10 | GSE61093 | GEO

NFIA Controls the Brown Fat Gene Program by Co-Localizing with PPARgamma at Cell-Type-Specific Enhancers (chromatin)

Project description:Brown fat dissipates energy as heat and protects against obesity. Here, we identified nuclear factor I-A (NFIA) as a novel transcriptional regulator of brown fat by a genome-wide open chromatin analysis of murine brown and white fat followed by motif analysis of brown-fat-specific open chromatin regions. NFIA and the adipogenic master regulator, PPARgamma, co-localize at the brown-fat-specific enhancers. Moreover, the binding of NFIA precedes and facilitates the binding of PPARgamma, leading to increased chromatin accessibility and active transcription. Introduction of NFIA into myoblasts results in brown adipocyte differentiation. Conversely, the brown fat of NFIA knockout mice displays impaired expression of the brown-fat-specific genes and reciprocal elevation of muscle genes. Finally, expression of NFIA and the brown-fat-specific genes is positively correlated in human brown fat. These results indicate that NFIA is a key transcriptional regulator of brown fat and exerts its effects by co-localizing with PPARg at cell-type-specific enhancers.

2017-08-14 | GSE83757 | GEO

NFIA Controls the Brown Fat Gene Program by Co-Localizing with PPARgamma at Cell-Type-Specific Enhancers (RNA)

Project description:Brown fat dissipates energy as heat and protects against obesity. Here, we identified nuclear factor I-A (NFIA) as a novel transcriptional regulator of brown fat by a genome-wide open chromatin analysis of murine brown and white fat followed by motif analysis of brown-fat-specific open chromatin regions. NFIA and the adipogenic master regulator, PPARγ, co-localize at the brown-fat-specific enhancers. Moreover, the binding of NFIA precedes and facilitates the binding of PPARγ, leading to increased chromatin accessibility and active transcription. Introduction of NFIA into myoblasts results in brown adipocyte differentiation. Conversely, the brown fat of NFIA knockout mice displays impaired expression of the brown-fat-specific genes and reciprocal elevation of muscle genes. Finally, expression of NFIA and the brown-fat-specific genes is positively correlated in human brown fat. These results indicate that NFIA is a key transcriptional regulator of brown fat and exerts its effects by co-localizing with PPARγ at cell-type-specific enhancers.

2017-08-14 | GSE83762 | GEO

RNA profiling to describe the transcriptional change during white fat browning, brown fat activity and inactivation

Project description:Enhancing brown fat activity and promoting white fat browning are attractive therapeutic strategies for obesity and its associated metabolic disorders. To provide a comprehensive picture of the regulatory network in these processes, we conducted a series of transcriptome studies by RNA-seq and quantified the mRNA and lncRNA changes during white fat browning induced by chronic cold exposure, beta-adrenergic agonist and intensive exercises, brown fat activation by acute cold exposure and inactivation by thermoneutrality.

2017-08-01 | GSE86338 | GEO

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