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The non-canonical SMC protein SmcHD1 antagonises TAD formation on the inactive X chromosome

ABSTRACT: The non-canonical SMC protein SmcHD1 antagonises TAD formation on the inactive X chromosome

PROVIDER: PRJNA476698 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6833530_1.fastq.gz	Fastqsanger.gz
	SRR6833530_2.fastq.gz	Fastqsanger.gz
	SRR6833540_1.fastq.gz	Fastqsanger.gz
	SRR6833540_2.fastq.gz	Fastqsanger.gz
	SRR6833550_1.fastq.gz	Fastqsanger.gz

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The non-canonical SMC protein SmcHD1 antagonises TAD formation on the inactive X chromosome (Repli-seq)

Project description:The non-canonical SMC protein SmcHD1 antagonises TAD formation on the inactive X chromosome (Repli-seq)

| PRJNA503902 | ENA

The non-canonical SMC protein SmcHD1 antagonises TAD formation and compartmentalisation on the inactive X chromosome.

Project description:The inactive X chromosome (Xi) in female mammals adopts an atypical higher-order chromatin structure, manifested as a global loss of local topologically associated domains (TADs), A/B compartments and formation of two mega-domains. Here we demonstrate that the non-canonical SMC family protein, SmcHD1, which is important for gene silencing on Xi, contributes to this unique chromosome architecture. Specifically, allelic mapping of the transcriptome and epigenome in SmcHD1 mutant cells reveals the appearance of sub-megabase domains defined by gene activation, CpG hypermethylation and depletion of Polycomb-mediated H3K27me3. These domains, which correlate with sites of SmcHD1 enrichment on Xi in wild-type cells, additionally adopt features of active X chromosome higher-order chromosome architecture, including A/B compartments and partial restoration of TAD boundaries. Xi chromosome architecture changes also occurred following SmcHD1 knockout in a somatic cell model, but in this case, independent of Xi gene derepression. We conclude that SmcHD1 is a key factor in defining the unique chromosome architecture of Xi.

| S-EPMC6318279 | biostudies-literature

The non-canonical SMC protein SmcHD1 antagonises TAD formation on the inactive X chromosome (Repli-seq)

Project description:In this study we investigate the role of the non-canonical SMC family protein, SmcHD1in the X inactivation.

2018-11-07 | GSE122196 | GEO

The non-canonical SMC protein SmcHD1 antagonises TAD formation on the inactive X chromosome

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-11-07 | GSE115984 | GEO

ATAC-seq 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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RRBS in Smchd1 control and Smchd1 deleted male and female neural stem cells.

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RNA-seq in Smchd1 wild-type and Smchd1 deleted differentiating male ES 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 loci. Smchd1 deletion in differentiating ES cells results in failed Hox gene silencing. 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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