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Genome-wide maps of PRDM16 binding sites and histone modifications [H3K4meChIP-Seq]

ABSTRACT: Identification of genome-wide PRDM16 binding, H3K27ac and H3K4me in WT and Prdm16 conditional knock-out (cKO) mouse (Emx1Ires-Cre; Prdm16flox/flox) at embryonic day 15.5.

ORGANISM(S): Mus musculus

PROVIDER: GSE111659 | GEO | 2018/06/21

REPOSITORIES: GEO

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Genome-wide maps of PRDM16 binding sites and histone modifications [PRDM16 ChIP-Seq]

Project description:Identification of genome-wide PRDM16 binding, H3K27ac and H3K4me in WT and Prdm16 conditional knock-out (cKO) mouse (Emx1Ires-Cre; Prdm16flox/flox) at embryonic day 15.5.

2018-06-21 | GSE111657 | GEO

Genome-wide maps of PRDM16 binding sites and histone modifications [H3K27Ac ChIP-Seq]

Project description:Identification of genome-wide PRDM16 binding, H3K27ac and H3K4me in WT and Prdm16 conditional knock-out (cKO) mouse (Emx1Ires-Cre; Prdm16flox/flox) at embryonic day 15.5.

2018-06-21 | GSE111658 | GEO

Transcriptome profiling of WT and Prdm16 mutant cells in embryonic mouse cerebral cortex.

Project description:Transcriptome profiling of radial glia, intermediate progenitors, and cortical neurons in WT and Prdm16 conditional knock-out (cKO) mouse (Emx1Ires-Cre; Prdm16flox/flox) at embryonic day 15.5.

2018-06-21 | GSE111660 | GEO

PRDM16 Functions as A Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle (bulk RNA-seq)

Project description:Gene expression profiling in whole heart, left ventricle (LV) and right ventricle (RV) of WT and Prdm16 conditional knockout (Prdm16cKO) mouse (Prdm16flox/flox; Xmlc2-Cre) at embryonic day 13.5 (E13.5).

2021-12-20 | GSE179386 | GEO

Genome-wide maps of PRDM16 binding sites and histone modifications [PRDM16 ChIP-Seq]

Project description:Genome-wide maps of PRDM16 binding sites and histone modifications [PRDM16 ChIP-Seq]

| PRJNA437763 | ENA

Genome-wide maps of PRDM16 binding sites and histone modifications

Project description:Genome-wide maps of PRDM16 binding sites and histone modifications

| PRJNA437760 | ENA

RNA-sequencing analysis of adult mouse wild type (Prdm16-Mx1-Cko/Cko; +/+) and Prdm16-/- (Prdm16-Mx1-Cko/Cko; Tg/+) Long Term-Hematopoietic Stem Cells (LT-HSC).

Project description:RNA-sequencing analysis of adult mouse wild type (Prdm16-Mx1-Cko/Cko; +/+) and Prdm16-/- (Prdm16-Mx1-Cko/Cko; Tg/+) Long Term-Hematopoietic Stem Cells (LT-HSC).

| PRJNA644817 | ENA

A methyltransferase EHMT1 controls brown adipose cell fate and adaptive thermogenesis through a PRDM16 complex

Project description:Brown adipose tissue (BAT) dissipates chemical energy in the form of heat, as a defense against hypothermia and obesity. Current evidence indicates that brown adipocytes arise from Myf5+-dermotomal precursors through the action of a PRDM16-C/EBP-_ transcriptional complex; however, the underlying mechanisms that determine lineage specification and maintenance of brown adipose cells remain poorly understood. Here we study the role of euchromatic histone-lysine N-methyltransferase 1 (EHMT1), a brown fat-enriched lysine methyltransferase, as an essential enzymatic component of the PRDM16 transcriptional complex and controls brown adipose cell fate. To identify targets and function of EHMT1, we performed genome-wide gene expression profiling of BAT from control mouce (Ehmt1flox/flox), Ehmt1Myf5 KO mouse (Myf5-Cre+/-; Ehmt1flox/flox) and Ehmt1adipo KO mouse (Adipo-Cre+/-; Ehmt1flox/flox). Loss of EHMT1 in Myf5+ lineage causes a near total loss of brown fat characteristics and induces muscle-selective gene program in vivo. In addition, adipose-specific deletion of EHMT1 by Adipo-Cre leads to a marked reduction of the thermogenic and fat oxidation genes.

2013-11-07 | E-MTAB-1704 | biostudies-arrayexpress

Genome-wide maps of PRDM16 binding sites and histone modifications [H3K4meChIP-Seq]

Project description:Genome-wide maps of PRDM16 binding sites and histone modifications [H3K4meChIP-Seq]

| PRJNA437762 | ENA

Prdm16 regulation of Shh-Gli1-Hoxc4 signaling is required for Granule Neuron Progenitor expansion and cerebellar related behavior

Project description:Purpose:To gain a deeper insight into how Prdm16 regulates cerebellar development, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by Prdm16 deletion at P3. Methods: Total RNA was extracted from P3 cerebellar tissue of Prdm16 cKO and Prdm16fl/fl mice. Then total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately approximately one thousand transcripts showed differential expression between the Prdm16fl/fl and Prdm16 cKO cerebellum, with a fold change ≥1.5 and p value <0.05. Gene ontology (GO) analysis showed that the down-regulated genes were enriched in the terms related to regulation of glial cell differentiation and forebrain development, and cerebellum development. Up-regulated genes showed a significant enrichment of terms involved in negative regulation of cell differentiation. These results reflected the importance of Prdm16 in cerebellar development. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding how Prdm16 gene contribute to cerebellar development.

2019-07-11 | GSE134091 | GEO

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