Xist RNA regulates remodeling of the Xi during B cell stimulation [RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA859802 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20281619_1.fastq.gz | Fastqsanger.gz | |||
| SRR20281619_2.fastq.gz | Fastqsanger.gz | |||
| SRR20281620_1.fastq.gz | Fastqsanger.gz | |||
| SRR20281620_2.fastq.gz | Fastqsanger.gz | |||
| SRR20281621_1.fastq.gz | Fastqsanger.gz |
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Project description:The inactive X (Xi) is formed by a process called X-Chromosome Inactivation (XCI), with Xist upregulation, retention of Xist RNA transcripts at the Xi, chromatin re-organization, and transcriptional silencing. Female lymphocytes have ‘dynamic’ XCI maintenance where Xist RNA is transcribed but absent from the Xi in naïve lymphocytes and re-localizes after in-vitro activation. How ‘dynamic’ XCI impacts Xi dosage and nuclear organization, or where Xist RNA interacts with the Xi is unknown. Here we find maintenance of Xi dosage and global structure despite the absence of Xist RNA in naïve B-cells. However, we identified 104 escape genes and observe a gain of de-novo TADs on the Xi. Stimulation-dependent Xi remodeling co-occurs with Xist RNA re-accumulation at the Xi, and loss of Xist increases TAD remodeling and decompacts the Xi in both naïve and stimulated B-cells. Altogether, these results reveal B-cell specific Xi plasticity which could underlie female-specific mechanisms in lymphocytes.
2024-12-31 | GSE208393 | GEO
Project description:The inactive X (Xi) is formed by a process called X-Chromosome Inactivation (XCI), with Xist upregulation, retention of Xist RNA transcripts at the Xi, chromatin re-organization, and transcriptional silencing. Female lymphocytes have ‘dynamic’ XCI maintenance where Xist RNA is transcribed but absent from the Xi in naïve lymphocytes and re-localizes after in-vitro activation. How ‘dynamic’ XCI impacts Xi dosage and nuclear organization, or where Xist RNA interacts with the Xi is unknown. Here we find maintenance of Xi dosage and global structure despite the absence of Xist RNA in naïve B-cells. However, we identified 104 escape genes and observe a gain of de-novo TADs on the Xi. Stimulation-dependent Xi remodeling co-occurs with Xist RNA re-accumulation at the Xi, and loss of Xist increases TAD remodeling and decompacts the Xi in both naïve and stimulated B-cells. Altogether, these results reveal B-cell specific Xi plasticity which could underlie female-specific mechanisms in lymphocytes.
2024-12-31 | GSE212257 | GEO
Project description:Xist RNA regulates remodeling of the Xi during B cell stimulation
| PRJNA890899 | ENA
Project description:Xist RNA regulates remodeling of the Xi during B cell stimulation [Hi-C]
| PRJNA874717 | ENA
Project description:The noncoding Xist RNA recruits silencing factors to the inactive X (Xi) and facilitates re-organization of Xi structure. Here, we examine the epigenomic landscape of the Xi and assess how Xist alters chromatin accessibility. Interestingly, Xist deletion propels selective chromatin re-accessibility on the Xi, affecting various Xi regions differentially. Re-accessibility is regulated by BRG1, an ATPase subunit of SWI/SNF chromatin remodeling complex. In vitro, RNA binding inhibits the nucleosome remodeling and ATPase activities of BRG1. In vivo, Xist directly interacts with BRG1 and expels BRG1 from the Xi. Xist ablation leads to a selective return of BRG1 in cis, emanating from pre-existing BRG1 sites that are Xist-free. BRG1's return correlates with cohesin re-binding and restoration of topologically associated domains (TADs), and results in formation of de novo Xi "superloops." Thus, Xist RNA binding inhibits BRG1's nucleosome remodeling activity and results in expulsion of the SWI/SNF complex from the Xi.
2019-01-14 | GSE109395 | GEO
Project description:The inactive X chromosome (Xi) serves as a model to understand gene silencing on a global scale. Here, we perform identification of direct RNA interacting proteins? (iDRiP) to isolate a comprehensive protein interactome for Xist, an RNA required for Xi silencing. We discover multiple classes of interactors, including cohesins, condensins, topoisomerases, RNA helicases, chromatin remodelers and modifiers, which synergistically repress Xi transcription. Inhibiting two or three interactors destabilizes silencing. While Xist attracts some interactors, it repels architectural factors. Xist evicts cohesins from the Xi and directs an Xi-specific chromosome conformation. Upon deleting Xist, the Xi acquires the cohesin-binding and chromosomal architecture of the active X. Our study unveils many layers of Xi repression and demonstrates a central role for RNA in the topological organization of mammalian chromosomes. The RNA-seq data sets generated in this study provide a resource for examining the effects of knockdowns of various Xist-interacting proteins on gene expression. The ChIP-seq data sets provide a comprehensive set of data examining CTCF and cohesion binding the X-chromosome, and the effects of deleting Xist on CTCF and cohesion binding. The Hi-C data is an allele-specific contact map of the X-chromosome higher-order chromatin structure in mouse. RNA-seq in 3 control and 10 knockdown cell lines. ChIP-seq for CTCF, Rad21 and Smc1a in wild-type fibroblasts and Xist-deletion fibroblasts. Hi-C in wild-type and Xist-deletion fibroblasts.
2015-06-19 | E-GEOD-67516 | biostudies-arrayexpress
Project description:X Chromosome Inactivation (XCI) is a female-specific process which balances X-linked gene dosage between sexes. Unstimulated T cells lack cytological enrichment of Xist RNA and heterochromatic modifications on the inactive X chromosome (Xi), and these modifications become enriched at the Xi after cell stimulation. Here, we examined allele-specific gene expression and epigenomic profiling of the Xi following T cell stimulation. We found that the Xi in unstimulated T cells is dosage compensated, and is enriched with the repressive H3K27me3 modification, but not H2AK119-ubiquitin (Ub) mark, including at promoters of XCI escape genes. Upon CD3/CD28 mediated T cell stimulation, the Xi accumulates H2AK119-Ub and H3K27me3 across the Xi. Next, we examined the T cell stimulation pathways responsible for Xist RNA localization to the Xi and found that T cell receptor (TCR) engagement, specifically NFkB signaling downstream of TCR, is required. Disruption of NFkB signaling, using inhibitors or genetic deletions, in mice and patients with immunodeficiencies prevents Xist/XIST RNA accumulation at the Xi and alters expression of some X-linked genes. Our findings reveal a novel connection between NFkB signaling pathways which impact XCI maintenance in female T cells.
2024-10-29 | GSE251882 | GEO
Project description:X Chromosome Inactivation (XCI) is a female-specific process which balances X-linked gene dosage between sexes. Unstimulated T cells lack cytological enrichment of Xist RNA and heterochromatic modifications on the inactive X chromosome (Xi), and these modifications become enriched at the Xi after cell stimulation. Here, we examined allele-specific gene expression and epigenomic profiling of the Xi following T cell stimulation. We found that the Xi in unstimulated T cells is dosage compensated, and is enriched with the repressive H3K27me3 modification, but not H2AK119-ubiquitin (Ub) mark, including at promoters of XCI escape genes. Upon CD3/CD28 mediated T cell stimulation, the Xi accumulates H2AK119-Ub and H3K27me3 across the Xi. Next, we examined the T cell stimulation pathways responsible for Xist RNA localization to the Xi and found that T cell receptor (TCR) engagement, specifically NFkB signaling downstream of TCR, is required. Disruption of NFkB signaling, using inhibitors or genetic deletions, in mice and patients with immunodeficiencies prevents Xist/XIST RNA accumulation at the Xi and alters expression of some X-linked genes. Our findings reveal a novel connection between NFkB signaling pathways which impact XCI maintenance in female T cells.
2024-10-29 | GSE251881 | GEO
Project description:X Chromosome Inactivation (XCI) is a female-specific process which balances X-linked gene dosage between sexes. Unstimulated T cells lack cytological enrichment of Xist RNA and heterochromatic modifications on the inactive X chromosome (Xi), and these modifications become enriched at the Xi after cell stimulation. Here, we examined allele-specific gene expression and epigenomic profiling of the Xi following T cell stimulation. We found that the Xi in unstimulated T cells is dosage compensated, and is enriched with the repressive H3K27me3 modification, but not H2AK119-ubiquitin (Ub) mark, including at promoters of XCI escape genes. Upon CD3/CD28 mediated T cell stimulation, the Xi accumulates H2AK119-Ub and H3K27me3 across the Xi. Next, we examined the T cell stimulation pathways responsible for Xist RNA localization to the Xi and found that T cell receptor (TCR) engagement, specifically NFkB signaling downstream of TCR, is required. Disruption of NFkB signaling, using inhibitors or genetic deletions, in mice and patients with immunodeficiencies prevents Xist/XIST RNA accumulation at the Xi and alters expression of some X-linked genes. Our findings reveal a novel connection between NFkB signaling pathways which impact XCI maintenance in female T cells.
2024-10-29 | GSE251880 | GEO
Project description:X Chromosome Inactivation (XCI) is a female-specific process which balances X-linked gene dosage between sexes. Unstimulated T cells lack cytological enrichment of Xist RNA and heterochromatic modifications on the inactive X chromosome (Xi), and these modifications become enriched at the Xi after cell stimulation. Here, we examined allele-specific gene expression and epigenomic profiling of the Xi following T cell stimulation. We found that the Xi in unstimulated T cells is dosage compensated, and is enriched with the repressive H3K27me3 modification, but not H2AK119-ubiquitin (Ub) mark, including at promoters of XCI escape genes. Upon CD3/CD28 mediated T cell stimulation, the Xi accumulates H2AK119-Ub and H3K27me3 across the Xi. Next, we examined the T cell stimulation pathways responsible for Xist RNA localization to the Xi and found that T cell receptor (TCR) engagement, specifically NFkB signaling downstream of TCR, is required. Disruption of NFkB signaling, using inhibitors or genetic deletions, in mice and patients with immunodeficiencies prevents Xist/XIST RNA accumulation at the Xi and alters expression of some X-linked genes. Our findings reveal a novel connection between NFkB signaling pathways which impact XCI maintenance in female T cells.
2024-10-29 | GSE251879 | GEO