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RNA-Seq of E14 MGE, Prdm16 WT vs cKO

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

PROVIDER: PRJNA670344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12855441_1.fastq.gz	Fastqsanger.gz
	SRR12855441_2.fastq.gz	Fastqsanger.gz
	SRR12855442_1.fastq.gz	Fastqsanger.gz
	SRR12855442_2.fastq.gz	Fastqsanger.gz
	SRR12855443_1.fastq.gz	Fastqsanger.gz

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RNA-Seq of E14 MGE, Prdm16 WT vs cKO

Project description:This study aimed to understand the role of the transcriptional regulator Prdm16 in the development of cortical interneurons in the mouse. Prdm16 was knocked out in cells derived from the medial ganglionic eminence (MGE) by using an Nkx2.1-Cre driver line in combination with a line carrying floxed Prdm16 alleles and with a Cre-dependent tdTomato reporter line (Ai14). The sequencing data compares the gene expression profiles of dissected MGEs at embryonic day 14 (E14), a stage when cortical interneurons are being generated from MGE progenitors.

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ChIP-Seq of PRDM16 binding sites in E14 MGE

Project description:ChIP-Seq of PRDM16 binding sites in E14 MGE

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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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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.

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