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In situ Hi-C in Smchd1 wild-type and Smchd1 deleted neural stem cells. [II]

ABSTRACT: In situ Hi-C in Smchd1 wild-type and Smchd1 deleted neural stem cells. [II]

PROVIDER: PRJNA476549 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7353823_1.fastq.gz	Fastqsanger.gz
	SRR7353823_2.fastq.gz	Fastqsanger.gz
	SRR7353824_1.fastq.gz	Fastqsanger.gz
	SRR7353824_2.fastq.gz	Fastqsanger.gz
	SRR7353825_1.fastq.gz	Fastqsanger.gz

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In situ Hi-C in Smchd1 wild-type and Smchd1 deleted neural stem cells.

Project description:In situ Hi-C in Smchd1 wild-type and Smchd1 deleted neural stem cells.

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In situ Hi-C in Smchd1 wild-type and Smchd1 deleted neural stem cells.

Project description:We sought to examine whether the non-canonical SMC protein Smchd1 plays a role in chromosome conformation. We used in situ Hi-C to analyse chromosome conformation changes upon deletion of the epigenetic regulator Smchd1 in female neural stem cells. In parallel, we analysed nucleosome accessibility using ATAC-seq, gene expression using RNA-seq, chromatin marks H3K27me3 and H3K27ac and Ctcf binding using ChIP-seq. We additionally analysed Smchd1 binding genome-wide using ChIP-seq. Together, we find that deletion of Smchd1 alters chromosome conformation at Smchd1 target genes including the inactive X chromosome, Hox genes and imprinted loc. Smchd1 deletion results in gain in Ctcf binding and activation of enhancers. We propose Smchd1 functions by limiting Ctcf-mediated chromosome looping.

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