UTX regulated genes in mouse embryonic stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE35415 | GEO | 2012/09/04
SECONDARY ACCESSION(S): PRJNA152573
REPOSITORIES: GEO
Similar Datasets
Project description:UTX gene is localized on the X chromosome, identified as a demethylase on histone H3 lysine 27. Two independent UTX conditional knockout (cKO) embryonic stem cell lines and two UTX knockout (KO) cell lines were cultured on 0.1% gelatin-coated dishes without feeder cells at desity of 1 million cells/10 cm dish. Cells were cultured overnight and collected. Total RNAs were sequentially purified with Trizol (Invitrogen) and RNeasy kit (Qiagen) and analyzed on Mouse Genome 430 2.0 Array (Affymetrix) at NIDDK Microarray Core Facility following standard protocols.
2012-09-04 | E-GEOD-35415 | biostudies-arrayexpress
Project description:UTX is a histone H3 lysine 27 demethylase required for development. However, the mechanisms underlying developmental gene regulation by UTX are unclear. Here, we discovered a molecular interaction between UTX and 53BP1 that regulates gene expression in a human neurogenesis model. Human 53BP1 contains a UTX-binding site that diverges from its mouse homolog by 41%, and our data suggest that the UTX-53BP1 interaction is conserved in primates but not rodents. ChIP-Seq revealed that the genome-wide targets of UTX and 53BP1 overlap by 84%. We used CRISPR-Cas9 to generate mutations of 53BP1 and UTX in human embryonic stem cells, and found that both 53BP1 and UTX are required to promote the expression of hundreds of neurogenic genes during neural differentiation. Further, 53BP1 is required for human neural progenitor differentiation into neurons. Our findings suggest that the UTX-53BP1 interaction controls gene expression important for neural differentiation in humans.
2019-02-15 | GSE108115 | GEO
Project description:UTX is a histone H3 lysine 27 demethylase required for development. However, the mechanisms underlying developmental gene regulation by UTX are unclear. Here, we discovered a molecular interaction between UTX and 53BP1 that regulates gene expression in a human neurogenesis model. Human 53BP1 contains a UTX-binding site that diverges from its mouse homolog by 41%, and our data suggest that the UTX-53BP1 interaction is conserved in primates but not rodents. ChIP-Seq revealed that the genome-wide targets of UTX and 53BP1 overlap by 84%. We used CRISPR-Cas9 to generate mutations of 53BP1 and UTX in human embryonic stem cells, and found that both 53BP1 and UTX are required to promote the expression of hundreds of neurogenic genes during neural differentiation. Further, 53BP1 is required for human neural progenitor differentiation into neurons. Our findings suggest that the UTX-53BP1 interaction controls gene expression important for neural differentiation in humans.
2019-02-15 | GSE108114 | GEO
Project description:Epigenetic changes, including histone methylation, control T cell differentiation and memory formation, though the enzymes that mediate these processes are not clear. We show that UTX, a histone H3 lysine 27 (H3K27) demethylase, promotes the generation of T follicular helper (Tfh) cells, a CD4+ T cell subset essential for B cell antibody generation and clearance of chronic viral infections. Mice with T cell specific UTX deletion (UTX TKO mice) had fewer Tfh cells, showed defective germinal center formation, lacked virus-specific IgG production, and were unable to resolve chronic lymphocytic choriomeningitis virus infection. In UTX TKO T cells, decreased expression of IL-6R±, and other Tfh-related loci, was associated with increased H3K27 methylation. Additionally, Turner Syndrome subjects, who are predisposed to chronic ear infections, have reduced UTX expression in immune cells and decreased Tfh frequency. Thus, we identify a critical link between UTX in T cells and immunity to infection. Mice were infected with chronic LCMV and sorted for Tfh on day 21 pi (sorted for: CD4+CXCR5+CD62Llo T cell). ChIP-Seq and RNA-Seq on WT and Utx KO cells.
2015-09-01 | E-GEOD-64969 | biostudies-arrayexpress
Project description:UTX is a histone H3 lysine 27 demethylase required for development. However, the mechanisms underlying developmental gene regulation by UTX are unclear. Here, we discovered a molecular interaction between UTX and 53BP1 that regulates gene expression in a human neurogenesis model. Human 53BP1 contains a UTX-binding site that diverges from its mouse homolog by 41%, and our data suggest that the UTX-53BP1 interaction is conserved in primates but not rodents. ChIP-Seq revealed that the genome-wide targets of UTX and 53BP1 overlap by 84%. We used CRISPR-Cas9 to generate mutations of 53BP1 and UTX in human embryonic stem cells, and found that both 53BP1 and UTX are required to promote the expression of hundreds of neurogenic genes during neural differentiation. Further, 53BP1 is required for human neural progenitor differentiation into neurons. Our findings suggest that the UTX-53BP1 interaction controls gene expression important for neural differentiation in humans.
2019-02-15 | GSE120333 | GEO
Project description:We describe inactivating somatic mutations in the histone lysine demethylase, UTX, in human cancers pointing to the deregulation of histone H3 lysine methylation in the development of multiple tumour types. Gene expression was analysed on Illumina Human WG-6 v2 BeadChips following standard protocols. Data quality test and normalization were performed using the Lumi package implemented in R.
2009-02-16 | E-MTAB-84 | biostudies-arrayexpress
Project description:Epigenetic changes, including histone methylation, control T cell differentiation and memory formation, though the enzymes that mediate these processes are not clear. We show that UTX, a histone H3 lysine 27 (H3K27) demethylase, promotes the generation of T follicular helper (Tfh) cells, a CD4+ T cell subset essential for B cell antibody generation and clearance of chronic viral infections. Mice with T cell specific UTX deletion (UTX TKO mice) had fewer Tfh cells, showed defective germinal center formation, lacked virus-specific IgG production, and were unable to resolve chronic lymphocytic choriomeningitis virus infection. In UTX TKO T cells, decreased expression of IL-6R±, and other Tfh-related loci, was associated with increased H3K27 methylation. Additionally, Turner Syndrome subjects, who are predisposed to chronic ear infections, have reduced UTX expression in immune cells and decreased Tfh frequency. Thus, we identify a critical link between UTX in T cells and immunity to infection.
2015-09-01 | GSE64969 | GEO
Project description:Lysine 9 di-methylation and lysine 27 tri-methylation of histone H3 (H3K9me2 and H3K27me3) are mostly linked to gene repression. However, functions of repressive histone methylation dynamics during inflammatory responses remain poorly understood. Here, we show that lysine demethylase 7A (KDM7A) and 6A (UTX) are rapidly transported to nuclear factor kappa-B (NF-κB) related elements in human endothelial cells in response to tumor necrosis factor (TNF)-α. KDM7A and UTX demethylate H3K9me2 and H3K27me3, respectively, and cooperatively activate NF-κB dependent inflammatory genes. Furthermore, using both in situ Hi-C and other 3C based technology, loops between super enhancers (SEs) are newly formed following TNF-α-stimuli at NF-κB-dependent inflammatory loci where KDM7A- and UTX-recruitment coincide. Collectively, these findings suggest that erasing of repressive histone marks by KDM7A and UTX within NF-κB-related elements might functionally associate with formation of SE-SE three-dimensional interactions and could be a cue signal during inflammatory responses in human endothelial cells.
2019-04-11 | GSE121890 | GEO
Project description:The UTX/KDM6A gene encodes the UTX histone H3K27 demethylase, which plays an important role in mammalian development and is frequently mutated in cancers and particularly, in urothelial cancers. Using BioID technique, we explored the interactome of different UTX isoforms.
2024-01-28 | PXD041254 | Pride
Project description:Pluripotency can be induced in somatic cells by ectopic expression of defined transcription factors, however the identity of epigenetic regulators driving the progression of cellular reprogramming requires further investigation. Here we uncover a non-redundant role for the JmjC-domain-containing protein histone H3 methylated Lys 27 (H3K27) demethylase Utx, as a critical regulator for the induction, but not for the maintenance, of primed and naM-CM-/ve pluripotency in mice and in humans. Utx depletion results in aberrant H3K27me3 repressive chromatin demethylation dynamics, which subsequently hampers the reactivation of pluripotency promoting genes during reprogramming. Remarkably, Utx deficient primordial germ cells (PGCs) display a cell autonomous aberrant epigenetic reprogramming in vivo during their embryonic maturation, resulting in the lack of functional contribution to the germ-line lineage. H3K27me3 and H3K4me3 were measured genome-wide in the following cell types: Utx+/Y (WT) and Utx-/Y (KO) mouse ES cells and mouse embryonic fibroblast (MEF) before and after DOX induction (initiating reprogramming by OSKM factors).
2012-05-30 | E-GEOD-37821 | biostudies-arrayexpress