Similar Datasets
Project description:X-chromosome inactivation (XCI) maintenance in female B cells is dynamic (dXCI), where naïve cells lack cytological enrichment of Xist RNA and heterochromatic marks on the inactive X-chromosome (Xi), and these marks re-localize after stimulation. Here, we report the epigenetic profiling of silencing (H3K27me3, H2AK119Ub, H3K9me3, DNA methylation (DNAm)) and activating (H3K27ac) marks on the Xi during dXCI and investigate the requirement for Xist RNA in maintaining the Xi epigenetic landscape. We find that the Xi in naïve B cells is depleted for H2AK119Ub and H3K9me3 but enriched for DNAm and H3K27me3 which maintain an epigenetic memory of transcriptional silencing dependent on Xist RNA. Upon stimulation, Xist-independent H3K27me3 and Xist-dependent H2AK119Ub modifications accumulate across the Xi. Thus, naïve B cells maintain an epigenetic memory of silencing in the absence of Xist RNA localization via retention of DNAm and H3K27me3, and both H3K27me3 and H2AK119Ub accumulate on the Xi post-stimulation in an Xist-dependent and -independent manner. These data have critical implications for understanding molecular mechanisms underlying female-biased immune responses.
2026-03-17 | GSE282256 | GEO
Project description:X-chromosome inactivation (XCI) maintenance in female B cells is dynamic (dXCI), where naïve cells lack cytological enrichment of Xist RNA and heterochromatic marks on the inactive X-chromosome (Xi), and these marks re-localize after stimulation. Here, we report the epigenetic profiling of silencing (H3K27me3, H2AK119Ub, H3K9me3, DNA methylation (DNAm)) and activating (H3K27ac) marks on the Xi during dXCI and investigate the requirement for Xist RNA in maintaining the Xi epigenetic landscape. We find that the Xi in naïve B cells is depleted for H2AK119Ub and H3K9me3 but enriched for DNAm and H3K27me3 which maintain an epigenetic memory of transcriptional silencing dependent on Xist RNA. Upon stimulation, Xist-independent H3K27me3 and Xist-dependent H2AK119Ub modifications accumulate across the Xi. Thus, naïve B cells maintain an epigenetic memory of silencing in the absence of Xist RNA localization via retention of DNAm and H3K27me3, and both H3K27me3 and H2AK119Ub accumulate on the Xi post-stimulation in an Xist-dependent and -independent manner. These data have critical implications for understanding molecular mechanisms underlying female-biased immune responses.
2026-03-17 | GSE282255 | GEO
Project description:X-chromosome inactivation (XCI) maintenance in female B cells is dynamic (dXCI), where naïve cells lack cytological enrichment of Xist RNA and heterochromatic marks on the inactive X-chromosome (Xi), and these marks re-localize after stimulation. Here, we report the epigenetic profiling of silencing (H3K27me3, H2AK119Ub, H3K9me3, DNA methylation (DNAm)) and activating (H3K27ac) marks on the Xi during dXCI and investigate the requirement for Xist RNA in maintaining the Xi epigenetic landscape. We find that the Xi in naïve B cells is depleted for H2AK119Ub and H3K9me3 but enriched for DNAm and H3K27me3 which maintain an epigenetic memory of transcriptional silencing dependent on Xist RNA. Upon stimulation, Xist-independent H3K27me3 and Xist-dependent H2AK119Ub modifications accumulate across the Xi. Thus, naïve B cells maintain an epigenetic memory of silencing in the absence of Xist RNA localization via retention of DNAm and H3K27me3, and both H3K27me3 and H2AK119Ub accumulate on the Xi post-stimulation in an Xist-dependent and -independent manner. These data have critical implications for understanding molecular mechanisms underlying female-biased immune responses.
2026-03-17 | GSE282254 | GEO
Project description:X-chromosome inactivation (XCI) maintenance in female B cells is dynamic (dXCI), where naïve cells lack cytological enrichment of Xist RNA and heterochromatic marks on the inactive X-chromosome (Xi), and these marks re-localize after stimulation. Here, we report the epigenetic profiling of silencing (H3K27me3, H2AK119Ub, H3K9me3, DNA methylation (DNAm)) and activating (H3K27ac) marks on the Xi during dXCI and investigate the requirement for Xist RNA in maintaining the Xi epigenetic landscape. We find that the Xi in naïve B cells is depleted for H2AK119Ub and H3K9me3 but enriched for DNAm and H3K27me3 which maintain an epigenetic memory of transcriptional silencing dependent on Xist RNA. Upon stimulation, Xist-independent H3K27me3 and Xist-dependent H2AK119Ub modifications accumulate across the Xi. Thus, naïve B cells maintain an epigenetic memory of silencing in the absence of Xist RNA localization via retention of DNAm and H3K27me3, and both H3K27me3 and H2AK119Ub accumulate on the Xi post-stimulation in an Xist-dependent and -independent manner. These data have critical implications for understanding molecular mechanisms underlying female-biased immune responses.
2026-03-17 | GSE282253 | GEO
Project description:X-chromosome inactivation (XCI) maintenance in female B cells is dynamic (dXCI), where naïve cells lack cytological enrichment of Xist RNA and heterochromatic marks on the inactive X-chromosome (Xi), and these marks re-localize after stimulation. Here, we report the epigenetic profiling of silencing (H3K27me3, H2AK119Ub, H3K9me3, DNA methylation (DNAm)) and activating (H3K27ac) marks on the Xi during dXCI and investigate the requirement for Xist RNA in maintaining the Xi epigenetic landscape. We find that the Xi in naïve B cells is depleted for H2AK119Ub and H3K9me3 but enriched for DNAm and H3K27me3 which maintain an epigenetic memory of transcriptional silencing dependent on Xist RNA. Upon stimulation, Xist-independent H3K27me3 and Xist-dependent H2AK119Ub modifications accumulate across the Xi. Thus, naïve B cells maintain an epigenetic memory of silencing in the absence of Xist RNA localization via retention of DNAm and H3K27me3, and both H3K27me3 and H2AK119Ub accumulate on the Xi post-stimulation in an Xist-dependent and -independent manner. These data have critical implications for understanding molecular mechanisms underlying female-biased immune responses.
2026-03-17 | GSE319172 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-06-17 | GSE119607 | GEO
Project description:XX female mammals undergo transcriptional silencing of most genes on one of their two X chromosomes to equalize X-linked gene dosage with XY males in a process referred to as X-chromosome inactivation (XCI). XCI is an example of epigenetic regulation. Once enacted in individual cells of the early female embryo, XCI is stably transmitted such that most descendant cells maintain silencing of that X chromosome. In eutherian mammals, XCI is thought to be triggered by the expression of the non-coding Xist RNA from the future inactive X chromosome (Xi); Xist RNA in turn is proposed to recruit protein complexes that bring about heterochromatinization of the Xi. Here we test whether imprinted XCI, which results in preferential inactivation of the paternal X chromosome (Xp), occurs in mouse embryos inheriting an Xp lacking Xist. We find that silencing of Xp-linked genes can initiate in the absence of paternal Xist; Xist is, however, required to stabilize silencing along the Xp. Xp-linked gene silencing associated with mouse imprinted XCI, therefore, can initiate in the embryo independently of Xist RNA.
| S-EPMC2754729 | biostudies-literature
Project description:During embryogenesis, the XIST RNA is expressed from and localizes to one X chromosome in females and induces chromosome-wide silencing. Although many changes to inactive X heterochromatin are known, the functional relationships between different modifications are not well understood, and studies of the initiation of X-inactivation have been largely confined to mouse. We now present a model system for human XIST RNA function in which induction of an XIST cDNA in somatic cells results in localized XIST RNA and transcriptional silencing. Chromatin immunoprecipitation and immunohistochemistry shows that this silencing need only be accompanied by a subset of heterochromatic marks and that these can differ between integration sites. Surprisingly, silencing is XIST-dependent, remaining reversible over extended periods. Deletion analysis demonstrates that the first exon of human XIST is sufficient for both transcript localization and the induction of silencing and that, unlike the situation in mice, the conserved repeat region is essential for both functions. In addition to providing mechanistic insights into chromosome regulation and formation of facultative heterochromatin, this work provides a tractable model system for the study of chromosome silencing and suggests key differences from mouse embryonic X-inactivation.
| S-EPMC1891207 | biostudies-literature
Project description:The non-coding RNA Xist regulates the process of X chromosome inactivation, in which one of the two X chromosomes present in cells of early female mammalian embryos is selectively and coordinately shut down. Remarkably Xist RNA functions in cis, affecting only the chromosome from which it is transcribed. This feature is attributable to the unique propensity of Xist RNA to accumulate over the territory of the chromosome on which it is synthesized, contrasting with the majority of RNAs that are rapidly exported out of the cell nucleus. In this review I provide an overview of the progress that has been made towards understanding localized accumulation of Xist RNA, drawing attention to evidence that some other non-coding RNAs probably function in a highly analogous manner. I describe a simple model for localized accumulation of Xist RNA and discuss key unresolved questions that need to be addressed in future studies.
| S-EPMC6936258 | biostudies-literature
Project description:Xist-mediated Chromosome Inactivation
| PRJNA489702 | ENA