Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Phosphorylation of the transcriptional-corepressor SPEN in naïve mouse embryonic stem cells and under artificial induction of X chromosome inactivation

ABSTRACT: We developed a CRISPR/Cas9-mediated base-editing screen to functionally screen endogenous proteins. We screened SPEN, a key factor in X chromosome inactivation, for loss-of-function mutations. Some of the screen hits were mutations of serine residues that could be potential phosphorylation sites (by prediction) and could serve as regulatory sites for the function and/or structure of SPEN. To follow up on our observations, we analyzed phosphorylation sites of SPEN in mouse embryonic stem cells, in which both X chromosomes are active (“noDox” sample), and in cells in which X chromosome inactivation was artificially induced by Xist expression (“Dox” sample).

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Embryonic Stem Cell

SUBMITTER: Corinne Kaufmann

LAB HEAD: Prof. Dr. Anton Wutz

PROVIDER: PXD073932 | Pride | 2026-04-08

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20250219_002_S887722_WT_noDox_enriched.d.zip	Other
	20250219_003_S887723_WT_Dox_enriched.d.zip	Other
	20250219_009_S887722_WT_noDox_proteome.d.zip	Other
	20250219_010_S887723_WT_Dox_proteome.d.zip	Other
	checksum.txt	Txt

Items per page:

1 - 5 of 9

Similar Datasets

XIST CHIRP-MS in GM12878 and K562 cell line

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

Xist-mediated Chromosome Inactivation

Project description:Xist-mediated Chromosome Inactivation

| PRJNA489702 | ENA

The role of Xist-mediated Polycomb recruitment in the initiation of X-chromosome inactivation

Project description:The role of Xist-mediated Polycomb recruitment in the initiation of X-chromosome inactivation

2019-08-29 | PXD014287 | Pride

Targeting microRNA-dependent control of X chromosome inactivation improves the Rett Syndrome phenotype

Project description:The X chromosome inactivation (XCI) is induced by Xist long non-coding RNA and protein-coding genes. However, the small non-coding RNA function in XCI remains unidentified. Our genome-wide, loss-of-function CRISPR/Cas9 screen in female fibroblasts examines the role of microRNA (miRNAs) in XCI. A striking finding is the identification of miR106a among the top candidates from 46 the screen. Loss of miR106a is accompanied by altered Xist interactome, leading to dissociation and destabilization of Xist. The XCI interference via miR106a inhibition has therapeutic implications for Rett syndrome (RTT) girls with a defective X-linked MECP2 gene. Here, we discovered that the genetic inhibition of miR106a significantly improves several facets of RTT pathology: it increases the life span, enhances locomotor activity and exploratory behavior, and diminishes breathing variabilities. Our results suggest that miR106a targeting offers a feasible therapeutic strategy for RTT and other monogenic X-linked neurodevelopmental disorders.

2026-02-09 | PXD064749 | Pride

The efficiency of Xist-mediated silencing of X-linked and autosomal genes is determined by the genomic environment

Project description:Xist is indispensable for X chromosome inactivation (XCI) in female mammalian cells. However, how Xist RNA directs chromosome-wide transcriptional inactivation of the X chromosome is largely unknown. Here, to study chromosome inactivation by Xist, we generated a system where ectopic Xist expression can be induced from several genomic contexts in aneuploid mouse ES cells. We found that ectopic Xist expression from any location on the X chromosome faithfully recapitulated endogenous XCI, showing the potency of Xist to initiate XCI. Genes that escape XCI remain consistently transcriptionally active upon ectopic XCI, regardless of their position relative to Xist transgenes, and the enrichment of CTCF at their promoters is implicated in directing XCI escape. Xist expression from autosomes facilitates their transcriptional silencing to different degrees, and gene density in proximity of the Xist transcription locus plays a central role in determining the efficiency of gene inactivation. We also show that the enrichment of LINE elements together with a specific chromatin environment facilitates Xist-mediated silencing of both X-linked and autosomal genes. These findings provide new insights into the epigenetic mechanisms that mediate XCI and identify genomic features that promote Xist-mediated chromosome-wide gene inactivation

2017-07-04 | GSE92894 | GEO

Escape from X inactivation is directly modulated by Xist non-coding RNA [methylation]

Project description:X-chromosome inactivation silences one copy of the X-chromosome in female cells, but a number of genes escapes this inactivation. We asked whether increased levels of Xist RNA, the molecular actor driving X-inactivation, impacts expression levels of escapees. To this end, we performed DNA methylation profiling of X-linked genes in clonal neural progenitor cell lines with transgenes that allow for the overexpression of Xist on the inactive X chromosome. We perform Xist overexpression experiments for up to three weeks and also test the reversibility of Xist overexpression using washout experiments.

2025-12-09 | GSE260483 | GEO

The role of XIST in X-inactivation maintenance in B cells (CRISPRi screen)

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

The role of XIST in X-inactivation maintenance in B cells (RNA-seq)

2021-01-12 | GSE164595 | GEO

The role of XIST in X-inactivation maintenance in B cells (ChIP-seq, Cut&Run))

2021-01-12 | GSE164594 | GEO

Escape from X inactivation is directly modulated by Xist non-coding RNA [cell line RNA-seq]

Project description:X-chromosome inactivation silences one copy of the X-chromosome in female cells, but a number of genes escapes this inactivation. We asked whether increased levels of Xist RNA, the molecular actor driving X-inactivation, impacts expression levels of escapees. To this end, we performed transcriptomic profiling of X-linked gene expression in clonal neural progenitor cell lines with transgenes that allow for the overexpression of Xist on the inactive X chromosome. We perform Xist overexpression experiments for up to three weeks and also test the reversibility of Xist overexpression using washout experiments. Finally, we demonstrate the role of SPEN in Xist-mediated silencing of escape using an inducible degron.

2025-12-09 | GSE259399 | GEO