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RNA-Seq of enriched astrocytes with MADM induced UPD of Chr. 7 (SMARTer)

ABSTRACT: RNA-Seq of enriched astrocytes with MADM induced UPD of Chr. 7 (SMARTer)

PROVIDER: PRJNA646267 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12222967.fastq.gz	Fastqsanger.gz
	SRR12222968.fastq.gz	Fastqsanger.gz
	SRR12222969.fastq.gz	Fastqsanger.gz
	SRR12222970.fastq.gz	Fastqsanger.gz
	SRR12222971.fastq.gz	Fastqsanger.gz

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RNA-Seq of MADM induced UPD of Chr. 7 (SMARTer)

Project description:RNA-Seq of MADM induced UPD of Chr. 7 (SMARTer)

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RNA-Seq of enriched astrocytes with MADM induced UPD of Chr. 7 (SMARTer)

Project description:In mammalian genomes a subset of genes is regulated by genomic imprinting resulting in silencing of one parental allele. Imprinting is essential for cerebral cortex development but prevalence and functional impact in individual cells is unclear. Here we determined allelic expression in cortical cell types and established a quantitative platform to interrogate imprinting in single cells. We created cells with uniparental disomy (UPD) containing either two copies of the maternal or paternal chromosome hence imprinted genes will be twofold overexpressed or not expressed. By genetic labeling of UPD we determined cellular phenotypes and transcriptional responses to deregulated imprinted gene expression at unprecedented single cell resolution. We discovered an unexpected degree of cell type specificity and a novel function of imprinting in the regulation of cortical astrocyte survival. More generally our results suggest functional relevance of imprinted gene expression in glial astrocyte lineage and thus for generating cortical cell type diversity.

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Project description:Mosaic Analysis with Double Markers (MADM) based glioma mouse model, which homozygously lacks Tp53 and Nf1, spontaneously developed gliomas at the post-natal 90-120 days. Tp53 and Nf1 are among the most frequently mutated genes in human glioma patients. Investigating the expression changes of genes induced by inactivation of Tp53, Nf1 and EZH2 can be a clue to clarify the mechanism of gliomagenesis. We examined the expressions of glioma cells in MADM mouse (n=2), EZH2 knocked-out MADM glioma tissues (n=3) and neural stem cell (NSC), astrocyte established with normal mice brains (n=2, respectively) and TP53 knocked-out astrocytes, derived from TP53 knocked-out mice (n=2). We used SurePrint G3 Mouse GE 8×60K array slides (G4858A, Agilent Technologies).

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