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Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation [ChIP-seq]

ABSTRACT: Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation [ChIP-seq]

PROVIDER: PRJNA439361 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6870752.fastq.gz	Fastqsanger.gz
	SRR6870753.fastq.gz	Fastqsanger.gz
	SRR6870754.fastq.gz	Fastqsanger.gz
	SRR6870755.fastq.gz	Fastqsanger.gz

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Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation

Project description:Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation

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Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation [RNA-seq]

Project description:Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation [RNA-seq]

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Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation [RNA-seq]

Project description:It has been shown that functional deficiency of SmcHD1, a noncanonical member of SMC family proteins, results in derepression of X-inactivated genes in postimplantation female mouse embryos. In this study, we found that derepression of X-inactivated genes accompanied a local reduction in the enrichment of H3K27me3 in mouse embryonic fibroblasts (MEFs) prepared from female fetuses deficient for SmcHD1.

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Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation [ChIP-seq]

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Investigating the role of SMCHD1 in de novo X chromosome inactivation

Project description:To investigate the effect of Smchd1 ablation on de novo X chromosome inactivation (XCI), we derived clonal neural progenitor cells (NPCs) from Smchd1+/+ (wild-type, WT) and Smchd1-/- mouse embryonic stem cells (ES cells; ESC). We generated allele-specific RNA-seq datasets from WT and Smchd1-/- NPCs to examine the effect of Smchd1 ablation on gene silencing. In addition, we produced allele-specific ChIP-seq profiles of H3K4me3, H3K27me3, CTCF, and RAD21 and Xist CHART-seq profiles in WT and Smchd1-/- NPCs to investigate the role of SMCHD1 on the distribution of euchromatin, facultative heterochromatin, architectural proteins, and Xist RNA on the inactive X chromosome (Xi). To determine the localization of SMCHD1 on the Xi, we employed allele-specific DamID-seq to map SMCHD1-binding regions in female mouse embryonic fibroblasts. Furthermore, we performed in situ Hi-C on WT NPCs, Smchd1-/- NPCs, and female ES cells undergoing XCI, in order to explore the role of SMCHD1 in regulating the higher-order structure of the Xi.

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Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation

Project description:Embryonic development is dependent on the maternal supply of proteins through the oocyte, including factors setting up the adequate epigenetic patterning of the zygotic genome. We previously reported that one such factor is the epigenetic repressor SMCHD1, whose maternal supply controls autosomal imprinted expression in mouse preimplantation embryos and mid-gestation placenta. In mouse preimplantation embryos, X chromosome inactivation is also an imprinted process. Combining genomics and imaging, we show that maternal SMCHD1 is required not only for the imprinted expression of Xist in preimplantation embryos, but also for the efficient silencing of the inactive X in both the preimplantation embryo and mid-gestation placenta. These results expand the role of SMCHD1 in enforcing the silencing of Polycomb targets. The inability of zygotic SMCHD1 to fully restore imprinted X inactivation further points to maternal SMCHD1's role in setting up the appropriate chromatin environment during preimplantation development, a critical window of epigenetic remodelling.

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Smchd1 dependent and independent pathways determine developmental dynamics of CpG island methylation on the inactive X chromosome.

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Project description:The function of Structural maintenance of chromosome flexible domain containing 1 (Smchd1) was examined during mouse preimplantation development using an siRNA knockdown approach. Transient SMCHD1 deficiency during the period between fertilization and morula/early blastocyst stage compromised embryo viability and resulted in reduced cell number, reduced embryo diameter, and reduced nuclear volumes at the morula stage. RNAseq analysis of Smchd1 knockdown morulae revealed aberrant increases in expression of mRNAs related to the trophoblast lineage, indicating SMCHD1 inhibits trophoblast lineage gene expression and promotes inner cell mass formation. siRNA knockdown also reduced expression of cell proliferation genes, including S-phase kinase-associated protein 2 (Skp2). Smchd1 expression was elevated in Caudal type homeobox transcription factor 2 (Cdx2)-/- blastocysts, indicating enriched expression, and further indicating a role in inner cell mass development. These results indicate that Smchd1 plays dual roles in the preimplantation embryo, promoting a lineage-appropriate pattern of gene expression supporting inner cell mass formation, whilst controlling lineage formation and gene expression in the trophectoderm.

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Role of SmcHD1 in the establishment of the epigenetic states required for the maintenance of X chromosome inactivation

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

2018-08-28 | GSE112097 | GEO

Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation

Project description:Maternal SMCHD1 controls both imprinted Xist expression and imprinted X chromosome inactivation

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