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Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

ABSTRACT: Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

PROVIDER: PRJNA1127522 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR29538832_1.fastq.gz	Fastqsanger.gz
	SRR29538832_2.fastq.gz	Fastqsanger.gz
	SRR29538834_1.fastq.gz	Fastqsanger.gz
	SRR29538834_2.fastq.gz	Fastqsanger.gz

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Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

Project description:Dysregulation of epigenetic mechanisms play crucial roles in brain development and disease. Emerging evidence suggests that RACK7, an epigenetic reader protein, may play a role in brain development, but in vivo exploration of RACK7 in neural development and the underlying mechanisms are still lacking. Here, we established a conditional knock-out Rack7 mouse model and show that Rack7-deficient mice exhibit overt developmental defects. Multicomplex immunofluorescence staining (mIF) of cell-type specific markers indicates that the developmental defects are associated with compromised astrocyte development. Mechanistically, we surprisingly found RACK7 interacts with PRC2 complex, which acts as the histone H3K27 methyltransferase. Our results suggest RACK7 binding with PRC2 complex helps to establish the proper genomic location of histone H3K27me3 modification. Deletion of Rack7 in astrocyte leads to a remarkable decrease of H3K27me3 chromatin enrichment. genome-wide?. Functionally, we found RACK7 works together with H3K27me3 to prevent overactivation of Wnt signaling pathway and other astrocyte differentiation genes. Collectively, our study provides new insights into the cellular and molecular mechanisms underlying brain development regulated by RACK7.

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Effects of deletion Rack7 on gene expression in primary astrocyte during mouse postnatal development [RNA-Seq]

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Project description:We identified that RACK7 recognizes the histone H3.3G34R mutaion in vitro. In order to determine the interaction between RACK7 and H3.3G34R mutaion in cells, we used three pediatric glioblastoma (pGBM) cell lines. SJ-HGGx6c(R6) and SJ-HGGx42c(R42) have heterozygous G34R mutation, while SJ-HGGx39c(WT39) has wildtype H3F3A, which encodes H3.3, and we also corrected H3.3G34R in R6 and R42 cells to wildtype H3.3 by CRISPR/Cas9 mediated knock-in. Finally, we performed RACK7 ChIP-seq in these cell lines to explore the function of RACK7 and H3.3G34R mutation.

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Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (ChIP-Seq Ring1b)

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Project description:Effects of deletion Rack7 on gene expression in primary astrocyte during mouse postnatal development [RNA-Seq]

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