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RNAseq of Wildtype, Smchd1 KO, Dux KO, Double KO, Tet-TKO and quadurple KO ES cells

ABSTRACT: RNAseq of Wildtype, Smchd1 KO, Dux KO, Double KO, Tet-TKO and quadurple KO ES cells

PROVIDER: PRJNA521986 | ENA |

REPOSITORIES: ENA

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RNAseq of Wildtype, Smchd1 KO, Dux KO, Double KO, Tet-TKO and quadurple KO ES cells

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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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RNAseq of DUX KO mouse 2-cell embryos

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Loss of DUX causes minor defects in zygotic genome activation and is compatible with mouse development

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