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Effects of loss and gain of KAT6B on gene expression in neural stem and progenitor cells [NSC_Kat6b_RNAseq]

ABSTRACT: Effects of loss and gain of KAT6B on gene expression in neural stem and progenitor cells [NSC_Kat6b_RNAseq]

PROVIDER: PRJNA1180534 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31181750_1.fastq.gz	Fastqsanger.gz
	SRR31181750_2.fastq.gz	Fastqsanger.gz
	SRR31181751_1.fastq.gz	Fastqsanger.gz
	SRR31181751_2.fastq.gz	Fastqsanger.gz
	SRR31181752_1.fastq.gz	Fastqsanger.gz

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Effects of loss and gain of KAT6B on gene expression in neural stem and progenitor cells [NSC_Kat6b_RNAseq]

Project description:High histone acetylation is associated with high transcriptional activity. The lysine acetyltransferase KAT6B is known to be required for histone acetylation and KAT6B is essential for normal brain development. In this study we examined the effects of loss and gain of KAT6B on gene expression in forebrain neural stem and progenitor cells (NSPCs). We isolated NSPCs from the dorsal telencephalon of embryonic day 12.5 embryos, which is the primordium of the cerebral cortex, from mouse embryos that lacked KAT6B or overexpressed KAT6B. We cultured the cells in vitro for 3 to 5 passages before isolating RNA for library production and RNA-sequencing. We found that genes required for neuronal differentiation and brain development were downregulated in Kat6b null cells and upregulated in Kat6b transgenic overexpressing cells.

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Project description:Heterozygous mutations in the histone acetyltransferase gene KAT6B (MYST4/MORF/QKF) cause cognitive disorders. Congruently, KAT6B is required for brain development, neural stem cell self-renewal and neuronal differentiation in mice. Despite the clear requirement for KAT6B in brain development, its molecular roles remain unexplored. Here we use ATAC sequencing to determine the effects of loss or gain of KAT6B on DNA accessiblity.

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