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Mus musculus

ABSTRACT: Analysis of hypertranscription in E13.5 mouse primordial germ cells

PROVIDER: PRJNA353006 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5008790.fastq.gz	Fastqsanger.gz
	SRR5008781.fastq.gz	Fastqsanger.gz
	SRR5008783.fastq.gz	Fastqsanger.gz
	SRR5008784.fastq.gz	Fastqsanger.gz
	SRR5008775.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:Transcriptome and epigenetic analysis in mouse primordial germ cells

| PRJDB3916 | ENA

Analysis of hypertranscription in E13.5 mouse primordial germ cells

Project description:During embryonic development, large-scale reprogramming occurs in primordial germ cells (PGCs) at the level of both DNA demethylation and histone modifications. While much is known about epigenetic changes, it still remains unclear how this chromatin state impacts the transcriptome and development of the germline. We have used cell-number normalised (CNN) RNA-seq to document the striking upregulation of the germ cell transcriptome at E13.5 compared to neighboring somatic cells of the embryonic gonad. We provide a novel, genome-wide analysis of hypertranscription during development, documenting the global amplification of the majority of the E13.5 PGC transcriptome. Upregulated transcripts in PGCs include those for ribosome biogenesis, translation and chromatin remodelling, as well as all transposable element families. These data reveal the significant hyperactivity of the germ cell transcriptome.

2017-06-06 | GSE89711 | GEO

Mus musculus

Project description:Characteristic energy metabolism in mouse primordial germ cells

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RNA-seq profiling of mouse PGC (Mus musculus)

Project description:PGCs undergo two distinct stages of demethylation before reaching a hypomethylated ground state at E13.5. Stage 1 occurs between E7.25- E9.5 in which PGCs experience a global loss of cytosine methylation. However, discreet loci escape this global loss of methylation and between E10.5-E13.5, stage 2 of demethylation takes place. In this stage these loci are targeted by Tet1 and Tet2 leading to the loss of the remaining methylation and resulting in the epigenetic ground state. Our data shows that Dnmt1 is responsible for maintaining the methylation of loci that escape stage 1 demethylation, and that it functions in a UHRF1 independent manner. Our data further demonstrates that when these loci lose methylation prior to stage 2 it results in early activation of the meiotic program, which leads to precocious differentiation of the germ line resulting in a decreased pool of PGCs in the embryo and subsequent infertility in adult mice.

2016-09-13 | GSE74938 | GEO

Mus musculus embryonic germ cell transcriptome

Project description:Identification of the mouse embryonic germ cell transcriptome

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Mus musculus Stra8-deficient fetal ovary transcriptome

Project description:Identification of the mouse embryonic germ cell Stra8-/- transcriptome

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Mus musculus Dazl-deficient fetal ovary transcriptome

Project description:Identification of the mouse embryonic germ cell Dazl-/- transcriptome

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H3K27me3 maintains the transcription program during epigenetic reprogramming in the mouse germ line [RNA-seq]

Project description:To investigate the role of EZH2 in transcription regulation in mouse primordial germ cells, we isolated Ctrl and Ezh2 CKO male and female PGCs at E13.5. Our data demonstrates that EZH2-mediated H3K27me3 is required for regulating the expression of meiotic genes in the female germ cells. Furthermore, RNA-seq analysis shows that EZH2 is essential for transcriptional repression of retrotransposons.

2021-09-27 | GSE141181 | GEO

Mus musculus strain:C57BL/6

Project description:Methylome of expanded mouse primordial germ cell-like cells

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Expression data from Mus musculus Myc-null heart at E13.5

Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null

2007-06-30 | GSE7162 | GEO

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