Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA Seq analysis of Mefs Isolated from STC1+/+ and STC1-/- mice

ABSTRACT: Evaluation of X-linked gene expression in MEFs isolated from STC1 wild type and knock out mice X chromosome inactivation (XCI) is initiated in cis by the Xist RNA, which coats the inactive X chromosome (Xi) from which it is produced. We performed a large-scale RNA interference screen to identify trans-acting XCI factors (XCIFs) that comprise regulators of cell signaling and transcription. We find that the XCIFs promote Xist expression and/or localization to the Xi. One of the XCIFs, STC1, is a glycoprotein found in both the cytoplasm and nucleus and whose function is poorly understood. A homozygous mouse knockout of STC1 has a defect in XCI but surprisingly is phenotypically normal. We performed transcriptome profiling (RNA-Seq) experiments to determine whether the expression levels of X-encoded genes were elevated in Stc1-/- female MEFs. In these experiments, RNA was prepared from three independent cultures of Stc1+/+ or Stc1-/- female MEFs. RNA samples were processed and amplified followed by deep sequencing. The similarity of X-linked gene expression between Stc1+/+ and Stc1-/- MEFs was statistically significant. The vast majority of autosomal genes were also expressed at comparable levels in Stc1+/+ and Stc1-/- MEFs.

ORGANISM(S): Mus musculus

PROVIDER: GSE47395 | GEO | 2014/07/29

SECONDARY ACCESSION(S): PRJNA205462

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA Seq analysis of Mefs Isolated from STC1+/+ and STC1-/- mice

Project description:Evaluation of X-linked gene expression in MEFs isolated from STC1 wild type and knock out mice X chromosome inactivation (XCI) is initiated in cis by the Xist RNA, which coats the inactive X chromosome (Xi) from which it is produced. We performed a large-scale RNA interference screen to identify trans-acting XCI factors (XCIFs) that comprise regulators of cell signaling and transcription. We find that the XCIFs promote Xist expression and/or localization to the Xi. One of the XCIFs, STC1, is a glycoprotein found in both the cytoplasm and nucleus and whose function is poorly understood. A homozygous mouse knockout of STC1 has a defect in XCI but surprisingly is phenotypically normal. We performed transcriptome profiling (RNA-Seq) experiments to determine whether the expression levels of X-encoded genes were elevated in Stc1-/- female MEFs. In these experiments, RNA was prepared from three independent cultures of Stc1+/+ or Stc1-/- female MEFs. RNA samples were processed and amplified followed by deep sequencing. The similarity of X-linked gene expression between Stc1+/+ and Stc1-/- MEFs was statistically significant. The vast majority of autosomal genes were also expressed at comparable levels in Stc1+/+ and Stc1-/- MEFs. Sequenced mRNA isolated from the STC1+/+ or STC1-/- MEFs.

2014-07-29 | E-GEOD-47395 | biostudies-arrayexpress

RNA-Seq analysis of murine splenic B cells with deletion of YY1

Project description:X chromosome inactivation (XCI) in female lymphocytes is uniquely regulated, as the inactive X (Xi) chromosome lacks localized Xist RNA and heterochromatin modifications. Epigenetic profiling reveals that Xist RNA is lost from the Xi at the pro-B cell stage and that additional heterochromatic modifications are gradually lost during B cell development. Activation of mature B cells restores Xist RNA and heterochromatin to the Xi in a dynamic two-step process that differs in timing and pattern, depending on the method of B cell stimulation. Finally, we find that DNA binding by YY1 maintains XCI in activated B cells, as ex-vivo YY1 deletion results in loss of Xi heterochromatin marks and up-regulation of X-linked genes. Ectopic expression of the YY1 zinc finger domain is sufficient for Xist RNA localization during B cell activation. Together, our results indicate that Xist RNA localization is critical for maintaining XCI in female lymphocytes, and that chromatin changes on the Xi during B cell development and the dynamic nature of YY1-dependent XCI maintenance in mature B cells predisposes X- linked immunity genes to reactivation.

2018-02-22 | GSE104097 | GEO

Copy number variant (CNV) and Single nucleotide polymorphism (SNP) of UCLA hESC lines

Project description:Female human ESC-lines can carry active X-chromosomes (Xa) or an XIST-RNA- coated inactive X-chromosome (Xi XIST+ ). Additionally, many ESC-lines have abnormal X-chromosome-inactivation (XCI)-states where the Xi no longer expresses XIST-RNA and has transcriptionally active regions (eroded Xi=Xe). The fate of each XCI-state upon differentiation is unclear because individual lines often contain a mixture of XCI-states. Here, we established homogeneous XiXa, XeXa, and XaXa ESC-lines. We found that these lines were unable to initiate XIST-expression and X-chromosome- wide silencing upon differentiation indicating that the ESC XCI-state is maintained in differentiated cells. Consequently, differentiated XeXa and XaXa cells displayed higher levels of X-linked gene-expression than XiXa cells. Although global transcriptional compensation between X-chromosomes and autosomes is not required for female ESC-differentiation, the degree of X-chromosome- silencing influences differentiation efficiencies. Our data suggest that the Xi XIST+ Xa state is inherent to human ESCs and that all other XCI-states, including XaXa, are abnormal and arise during ESC-derivation or maintenance.

2016-12-15 | GSE91072 | GEO

NFkB Signaling is Required for Xist RNA Localization at the Inactive X and for X-Chromosome Inactivation Maintenance Following T cell Activation [CUT&Run]

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 | GSE268526 | GEO

NFkB Signaling is Required for Xist RNA Localization at the Inactive X and for X-Chromosome Inactivation Maintenance Following T cell Activation [RNAseq_ESCAPE_nfkb]

2024-10-29 | GSE251880 | GEO

NFkB Signaling is Required for Xist RNA Localization at the Inactive X and for X-Chromosome Inactivation Maintenance Following T cell Activation [RNAseq_geneexpression]

2024-10-29 | GSE251882 | GEO

NFkB Signaling is Required for Xist RNA Localization at the Inactive X and for X-Chromosome Inactivation Maintenance Following T cell Activation [RNAseq_ESCAPE_stimulation]

2024-10-29 | GSE251881 | GEO

NFkB Signaling is Required for Xist RNA Localization at the Inactive X and for X-Chromosome Inactivation Maintenance Following T cell Activation [CUT&RUN]

2024-10-29 | GSE251879 | GEO

SPEN is required for Xist upregulation during initiation of X chromosome inactivation (RNA-seq)

Project description:At initiation of X chromosome inactivation (XCI), Xist is monoallelically upregulated from the future inactive X (Xi) chromosome, overcoming repression by its antisense transcript Tsix. Xist recruits various chromatin remodelers, amongst them SPEN, which are involved in silencing of X-linked genes in cis and establishment of the Xi. Here, we show that SPEN plays an important role in the initiation of XCI. Spen null female mouse embryonic stem cells (ESCs) are defective in Xist upregulation upon differentiation. We find that Xist-mediated SPEN recruitment to the Xi chromosome happens very early in XCI, and that SPEN-mediated silencing of the Tsix promoter is required for Xist upregulation. Accordingly, failed Xist upregulation in Spen-/- ESCs can be rescued by concomitant removal of Tsix. These findings indicate that SPEN is not only required for the establishment of the Xi, but is also crucial in the initiation of the XCI process.

2021-09-30 | GSE163320 | GEO

SPEN is required for Xist upregulation during initiation of X chromosome inactivation (ChIP-seq)

2021-09-30 | GSE163319 | GEO