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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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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 [ChIP-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 [RNA-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.

Project description:X chromosome inactivation involves multiple levels of chromatin modification, established progressively and in a stepwise manner during early development. The chromosomal protein Smchd1 has recently been shown to play an important role in DNA methylation of CpG islands (CGIs), a late step in the X inactivation pathway required for long-term stability of gene silencing. Here we show that inactive X chromosome (Xi) CGI methylation can occur via either Smchd1 dependent or independent pathways. Smchd1 dependent CGI methylation, the primary pathway, is acquired gradually over an extended period, whereas Smchd1 independent CGI methylation occurs rapidly after the onset of X inactivation. The de novo methyltransferase Dnmt3b is required for methylation of both classes of CGI, whereas Dnmt3a and Dnmt3L are dispensable. Xi CGIs methylated by these distinct pathways differ in respect to their sequence characteristics and immediate chromosomal environment. We discuss the implications of these results for understanding CGI methylation during development. Examination of CpG methylated DNA from wild type and smchd1 null male and female somatic cells and female ES cells differentiated for either 7 or 10 days. Duplicate samples of each type were generated.

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Roles of Structural maintenance of chromosome flexible domain containing 1 (Smchd1) in early lineage formation and development in mice

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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

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

2012-10-15 | GSE37333 | GEO