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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE111660 | 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 [H3K4meChIP-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 | GSE111659 | 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

RNA-seq analysis of Wildtype and Prdm16 cKO ventricular zone tissue during cortex development in mouse

Project description:Purpose: To explore the mechanisms by which PRDM16 regulates reactive oxygen species levels and oxidative stress in radial glia progenitors during cortical development in mouse.

2020-02-16 | GSE142684 | GEO

Changes in DNA methylation upon gain and loss of Prdm16 function

Project description:Cortical neurogenesis requires the fine tuning of gene expression, modulated by genetic and epigenetic mechanisms during the entire process. Among the epigenetic factors expressed by the proliferative radial glia cells, Prdm16 has been shown to play a key role in cell proliferation. We found Prdm16 to be expressed exclusively by radial glia cells and to be rapidly turned off in newborn neurons. Predictably, Prdm16-null mice displayed a decrease in cortical thickness as a consequence of an impairment in self-renewal of radial glia cells. Conversely, Prdm16-overexpressing neural progenitors showed an increase in self-renewal activity and failed to complete differentiation. Lineage restriction in differentiating stem cells is achieved by chromatin modifications such as histone modifications and DNA methylation along the promoters of stemness-related genes. We found the expression of the DNA methyltransferase Dnmt3b to be inversely correlated to that of Prdm16. Loss and gain of Prdm16 function leaded to an up- and down-regulation of Dnmt3b, respectively. Functional analysis confirmed Prdm16 competence to repress Dnmt3b expression. Finally, IUE of Prdm16 together with Dnmt3b rescued the increase in radial glia cells self-renewal observed with Prdm16 alone. Thus, Prdm16 may play a crucial role in ensuring neural progenitor self-renewal, mainly through the maintenance of the unmethylated state of stemness-related genes.

2022-05-25 | GSE59574 | GEO

Changes in DNA methylation upon gain and loss of Prdm16 function (MeDIP-seq)

2022-05-25 | GSE77697 | 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).

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PRDM16 regulates a temporal transcriptional program to promote progression of cortical neural progenitors

Project description:Radial glia (RG) in the neocortex sequentially generate distinct subtypes of projection neurons, accounting for the diversity and complex assembly of cortical neural circuits. Mechanisms that drive the rapid and precise temporal progression of RG are beginning to be elucidated. Here we reveal that the RG-specific transcriptional regulator PRDM16 promotes the transition of early to late phase of neurogenesis in the mouse neocortex. Loss of Prdm16 delays the timely progression of RG, leading to defective cortical laminar organization. Our genomic analyses demonstrate that PRDM16 regulates a subset of genes that are dynamically expressed between early and late neurogenesis. We show that PRDM16 suppresses target gene expression through limiting chromatin accessibility of permissive enhancers. We further confirm that critical target genes regulated by PRDM16 comprise neuronal specification genes, cell cycle regulators and molecules required for neuronal migration. These findings provide evidences to support that neural progenitors temporally shift gene expression program to achieve neural cell diversity.

2021-03-03 | GSE162854 | GEO

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

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