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

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

PROVIDER: PRJNA597923 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10798652_1.fastq.gz	Fastqsanger.gz
	SRR10798652_2.fastq.gz	Fastqsanger.gz
	SRR10798653_1.fastq.gz	Fastqsanger.gz
	SRR10798653_2.fastq.gz	Fastqsanger.gz
	SRR10798654_1.fastq.gz	Fastqsanger.gz

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Prdm16 newborn mouse (ventricular zone) VZ cells microarray

Project description:As Prdm16 deficiency reduces self-renewal potential and depletes neural stem cells in culture we decided to investigate the underlying molecular mechanisms of the neural stem cells depletion in the Prdm16 deficient animals. For the experiment we used Prdm16Gt(OST67423)Lex (Prdm16LacZ) genetrap mice obtained from the NIH Mutant Mouse Regional Resource Center (http://www.mmrrc.org/). We compared the gene expression profiles of uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ (KO), Prdm16LacZ/+(HET), and Prdm16+/+ (WT) mice. The uncultured ventricular zone cells from newborn Prdm16LacZ/LacZ, Prdm16LacZ/+, and Prdm16+/+ mice were dissected from the brains and placed into the Trizol reagent. Purified RNA was reverse transcribed and amplified using the WT-Ovation™ Applause WT/Amp RNA amplification system (NuGEN Technologies,) following the manufacturer’s instructions. Sense strand cDNA was fragmented and labeled using the FL-Ovation™ cDNA Biotin Module V2 (NuGEN). 2.5µg of labeled cDNA were hybridized to Affymetrix Mouse Gene ST 1.0 microarrays.

2010-09-09 | E-GEOD-23406 | biostudies-arrayexpress

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.

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2010-09-09 | GSE23406 | 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).

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PRDM16 is required for proper specification of the working ventricular myocardium by suppressing alternative cardiomyocyte cell fates.

Project description:PRDM16 is a transcription factor with histone methyltransferase activity expressed at the earliest stages of cardiac development. Pathogenic mutations in humans lead to cardiomyopathy, conduction abnormalities and heart failure. PRDM16 is specifically expressed in ventricular but not atrial cardiomyocytes and declines in expression postnatally. Since in other tissues PRDM16 is best known for its role in binary cell fate decisions, we hypothesized a similar decision-making function in cardiomyocytes. Here, we demonstrated that cardiomyocyte-specific deletion of Prdm16 during cardiac development results in contractile dysfunction and abnormal electrophysiology of the postnatal heart, resulting in premature death. By combined RNA+ATAC single-cell sequencing we found that PRDM16 favors ventricular working cardiomyocyte identity, by opposing the activity of master regulators of atrial and ventricular conduction fate. Myocardial loss of Prdm16 during development resulted in hyperplasia of the ventricular conduction system. Hence, PRDM16 plays an indispensable role during cardiac development by driving ventricular working cardiomyocyte identity.

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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:Regulation of quiescence is critical for the maintenance of adult hematopoietic stem cells (HSCs). Previous studies by gene disruption during mouse embryonic development have shown that transcription factor gene Prdm16 is important for the generation/maintenance of fetal liver HSCs; however, the underlying mechanisms and the function of Prdm16 in adult HSCs remain unclear. To investigate the role of Prdm16 in adult HSCs, we generated a novel conditional knockout mouse model and deleted Prdm16 in adult mouse hematopoietic system using the interferon inducible Mx1-Cre. Our results show that deletion of Prdm16 leads to a gradual decline of adult HSC numbers and a concomitant increase in the multipotent progenitor (MPP) compartment. Prdm16 deletion in the hematopoietic system following transplantation produced the same phenotype indicating that the defect is intrinsic to the HSCs. This HSC loss was also exacerbated by stress induced by 5-FU injections. Annexin V staining showed no difference in apoptosis between wild type and knockout HSCs. In contrast, BrdU analysis revealed that loss of Prdm16 significantly increases cycling of long-term HSCs (LT-HSCs) with majority of the cells found in the S to G2/M phase. Consistently, RNA-seq analysis of mouse LT- HSCs with and without Prdm16 deletion showed that Prdm16 loss induced a significant decrease in the expression of several known cell cycle regulators of HSCs, among which Cdkn1a and Egr1 were further identified as direct targets of Prdm16. Our results suggest that Prdm16 preserves the function of adult LT-HSCs by promoting their quiescence.

2021-11-22 | GSE154011 | GEO

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

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

RNA-Seq of E14 MGE, Prdm16 WT vs cKO

Project description:RNA-Seq of E14 MGE, Prdm16 WT vs cKO

| PRJNA670344 | ENA

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

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