A role for the GATA transcription factor family in X-chromosome inactivation as direct potent Xist activators
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA798737 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17665667_1.fastq.gz | Fastqsanger.gz | |||
| SRR17665667_2.fastq.gz | Fastqsanger.gz | |||
| SRR17665668_1.fastq.gz | Fastqsanger.gz | |||
| SRR17665668_2.fastq.gz | Fastqsanger.gz | |||
| SRR17665669_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 76 |
Similar Datasets
Project description:As the master regulator of X-chromosome inactivation (XCI), the Xist RNA is expressed nearly ubiquitously in female mice. Xist is only absent in the germ line and at the pluripotent state. Xist is generally assumed to be expressed “by default” in females, while being actively repressed in the few tissues where it is silent. Whether activating mechanisms also contribute remained largely unknown. Through a pooled CRISPR screen we identify the GATA family of transcription factors as potent direct activators of Xist. We describe a GATA-responsive regulatory element (RE79), located ~100 kb upstream of the Xist promoter. In cell lines derived from the two extraembryonic lineages, XEN and TS cells, where imprinted Xist expression is maintained, RE79 is bound by different sets of GATA factors expressed in those tissues. Here we use a CRISPR activation screen targeting X-chromosomal genes on differentiating XO mouse embryonic stem cells to identify putative Xist activators.
2022-01-26 | GSE194013 | GEO
Project description:As the master regulator of X-chromosome inactivation (XCI), the Xist RNA is expressed nearly ubiquitously in female mice. Xist is only absent in the germ line and at the pluripotent state. Xist is generally assumed to be expressed “by default” in females, while being actively repressed in the few tissues where it is silent. Whether activating mechanisms also contribute remained largely unknown. Through a pooled CRISPR screen we identify the GATA family of transcription factors as potent direct activators of Xist. We describe a GATA-responsive regulatory element (RE79), located ~100 kb upstream of the Xist promoter. In cell lines derived from the two extraembryonic lineages, XEN and TS cells, where imprinted Xist expression is maintained, RE79 is bound by different sets of GATA factors expressed in those tissues. Here we use CUT&Tag on GATA factors to profile their involvement at the X inactivation center in XEN and TS cells.
2022-01-26 | GSE194014 | GEO
Project description:Xist-mediated Chromosome Inactivation
| PRJNA489702 | ENA
Project description:The role of Xist-mediated Polycomb recruitment in the initiation of X-chromosome inactivation
2019-08-29 | PXD014287 | Pride
Project description:As the master regulator of X-chromosome inactivation (XCI), the Xist RNA is expressed nearly ubiquitously in female mice. Xist is only absent in the germ line and at the pluripotent state. Xist is generally assumed to be expressed “by default” in females, while being actively repressed in the few tissues where it is silent. Whether activating mechanisms also contribute remained largely unknown. Through a pooled CRISPR screen we identify the GATA family of transcription factors as potent direct activators of Xist. We describe a GATA-responsive regulatory element (RE79), located ~100 kb upstream of the Xist promoter. In cell lines derived from the two extraembryonic lineages, XEN and TS cells, where imprinted Xist expression is maintained, RE79 is bound by different sets of GATA factors expressed in those tissues. Here we use RNA-seq on differentiating XO mouse embryonic stem cells as a reference for gene expression during early differentiation.
2022-01-26 | GSE194016 | GEO
Project description:X-chromosome aneuploidies have long been associated with human cancers, but causality has not been established. In mammals, X-chromosome inactivation (XCI) is triggered by Xist RNA to equalize gene expression between the sexes. Here we delete Xist in the blood compartment of mice and demonstrate that mutant females develop a highly aggressive myeloproliferative neoplasm and myelodysplastic syndrome (mixed MPN/MDS) with 100% penetrance. Significant disease components include primary myelofibrosis, leukemia, histiocytic sarcoma, and vasculitis. Xist-deficient hematopoietic stem cells (HSC) show aberrant maturation and age-dependent loss. Reconstitution experiments indicate that MPN/MDS and myelofibrosis are of hematopoietic rather than stromal origin. We propose that Xist loss results in X-reactivation and consequent genome-wide changes that lead to cancer, thereby causally linking the X-chromosome to cancer in mice. Thus, Xist RNA is not only required to maintain XCI but also suppresses cancer in vivo. We carried out expression profiling in hematopoietic cells isolated from Xist-deficient female mice before disease (2 months old) and during myeloprolifeative neoplasm/myelodysplastic syndrome (MPN/MDS) and chronic myelomonocytic leukemia (CMML)-like disease (6 and 12 months old) and compared profiles of purified bone marow HSCs (KLS+CD34-), splenic B-cells (B220+), myeloid cells (CD11b+), and erythroid cells (Ter119+) against those of corresponding cell types from age-matched wild-type female mice. We conditionally targeted Xist locus in the blood compartment of mice by crossing Xist2lox/2lox mice (129Sv/Jae; Csankovszki et al., 1999) with Vav.Cre mice (B6.Cg-Tg (Vav1-cre)A2Kio/J; Jackson Laboratory). We used hematopoietic cells that were isolated from Xist-deficient and wild-type female progeny to analyze changes in gene expression due to loss of Xist.
2013-02-20 | E-GEOD-43961 | biostudies-arrayexpress
Project description:Mammals have evolved a mechanism to compensate for the difference in the number of X chromosome genes between XX females and XY males by inactivating one of the two X chromosomes in females. This X chromosome inactivation phenomenon is triggered by Xist gene, which is essential for X-inactivation to occur in cis. We demonstrate that an Xist mutant, XistIVS, is unique in that it retains a partial function to silence the X chromosome, which would provide an opportunity to dissect the molecular mechanism of Xist RNA-mediated chromosome silencing. To study the effect of XistIVS mutation on silencing of X-linked genes, global expression levels of X-linked genes were measured in mutant and control cells. We used female trophoblast stem (TS) cells carrying XistIVS mutation and gene expression was assayed using microarray containing 572 probes corresponding most of the X-linked genes. Then the result was compared with that obtained from wild-type control cells.
2011-03-30 | E-GEOD-27373 | biostudies-arrayexpress
Project description:Identification of cell type-specific XIST co-factors during maintenance of X chromosome inactivation by XIST CHIRP-MS
2021-03-08 | PXD023516 | Pride
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-01-26 | GSE194018 | GEO
Project description:The long noncoding RNA (lncRNA) XIST establishes X chromosome inactivation (XCI) in female cells in early development and thereafter is thought to be largely dispensable. Here we show XIST is continually required in adult human B cells to silence a subset of X-linked immune genes such as TLR7. XIST-dependent genes lack promoter DNA methylation and require continual XIST-dependent histone deacetylation. XIST RNA-directed proteomics and CRISPRi screen reveal distinctive somatic cell-specific XIST complexes, and identify TRIM28 that mediates Pol II pausing at promoters of X-linked genes in B cells. XIST dysregylation, reflected by escape of XIST-dependent genes, occurs in CD11c+ atypical memory B cells across single-cell transcriptome data in patients with female-biased autoimmunity and COVID-19 infection. XIST inactivation with TLR7 agonism suffices to promote isotype-switched atypical B cells. These results suggest cell-type-specific diversification of lncRNA-protein complexes increase lncRNA functionalities, and expand roles for XIST in sex-differences in biology and medicine.
2021-01-12 | GSE164593 | GEO