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RACK7 ChIP-seq in pediatric glioblastomas cell lines.

ABSTRACT: RACK7 ChIP-seq in pediatric glioblastomas cell lines.

PROVIDER: PRJNA574409 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10191302_1.fastq.gz	Fastqsanger.gz
	SRR10191302_2.fastq.gz	Fastqsanger.gz
	SRR10191303_1.fastq.gz	Fastqsanger.gz
	SRR10191303_2.fastq.gz	Fastqsanger.gz
	SRR10191304_1.fastq.gz	Fastqsanger.gz

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RACK7 ChIP-seq in pediatric glioblastomas cell lines.

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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Project description:Histone H3 point mutations have recently been identified in pediatric brain cancers, including missense mutations on histone H3 at positions 27 (lysine to methionine; K27M) and 34 (glycine to arginine, G34R), respectively. H3K27M mutations are associated with a majority of pediatric Diffuse Intrinsic Pontine Pediatric Glioma (DIPG) cases, while H3.3G34R is found in pediatric glioblastoma (GBM) arising in the cerebral cortex1,2. While the mechanisms of H3K27M-driven tumorigenesis are beginning to unravel, much less is known about the H3.3G34R mutation. Here, we provide both biochemical and structural evidence that the PHD (plant homedomain) domain of the enhancer-binding protein, RACK7 (ZMYND8), recognizes H3.3G34R mutant histone via a mechanism distinct from other PHD domains. In an H3.3G34R-expressing neuronal precursor cell line, we demonstrate that RACK7 is aberrantly recruited to enhancers bound by H3.3G34R, resulting in the down-regulation of many neuronal genes, and the up-regulation of oncogenes such as MYC. Neural precursor cells expressing H3.3G34R showed enhanced tumor growth when injected subcutaneously. Inhibiting RACK7 binding to H3.3G34R reduces tumor size and alters gene expression, suggesting that H3.3G34R regulation of enhancers via RACK7 promotes tumorigenesis. Specifically, we show that both the gene expression and tumor size regulation are critically dependent on the physical interaction of H3.3G34R with RACK7. Both regulations are compromised in the absence of RACK7, and can be rescued by wildtype, but not an H3.3G34R-binding defective, RACK7. Taken together, we have identified a reader for H3.3G34R and demonstrate that RACK7 binding to H3.3G34R alters enhancer activity to directly suppress neural gene transcription and to increase oncogenic propensity of neural precursor cells, thus providing a potential molecular basis for pediatric GBM driven by the H3.3G34R mutation.

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