Genome-wide epigenome mapping in human induced pluripotent cells in WT and KDM6KO cells. [ChIP-Seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE168249 | GEO | 2022/03/03
REPOSITORIES: GEO
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Project description:KDM6A is a histone demethylase that remove H3K27me3 lysine. This study compares the transcriptomic profile between WT and KDM6A KO cells and further evaluates their functional validation by applying the invitro hematopoietic differentiation protocol.
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Project description:KMT2C is a histone methyltransferase that mono-methylates lysine four at enhancer regions. This study compares the histone modification pattern between WT and KMT2C KO cells and further evaluates their functional validation by applying the invitro hematopoietic differentiation protocol.
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Project description:KMT2C is a histone methyltransferase that mono-methylates lysine four at enhancer regions. This study compares the transcriptomic profile between WT and KMT2C KO cells and further evaluates their functional validation by applying the invitro hematopoietic differentiation protocol.
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Project description:KMT2C is a histone methyltransferase that mono-methylates lysine four at enhancer regions. This study compares the open and closed chromatin region between WT and KMT2C KO cells and further evaluates their functional validation by applying the invitro hematopoietic differentiation protocol.
2021-04-01 | GSE158917 | GEO
Project description:Here we show binding and occupancy profiles for KDM6A, H3K27me3 and H3K4me3 to address the epigenetic regulation of a subset of Rhox genes, Rhox6 and 9, in female and male ES cells during differentiation. To further address a functional role for KDM6A in the epigenetic regulation of Rhox6 and 9, binding profiles for female ES cells treated with a control siRNA and siRNA specific for Kdm6a are shown. We report that two members of the Rhox cluster, Rhox6 and 9, are regulated by de-methylation of histone H3 at lysine 27 by KDM6A, a histone demethylase with female-biased expression. Our results are consistent with other homeobox genes in that Rhox6 and 9 are in bivalent domains prior to embryonic stem cell differentiation and thus poised for activation. In female mouse ES cells KDM6A is specifically recruited to Rhox6 and 9 for gene activation, a process inhibited by Kdm6a knockdown. In contrast, KDM6A occupancy at Rhox6 and 9 is low in male ES cells and knockdown has no effect on expression. Our study implicates Kdm6a, a gene that escapes X inactivation, in the regulation of genes important in reproduction, suggesting that KDM6A may play a role in the etiology of developmental and reproduction-related effects of X chromosome anomalies. ChIP-chip was used to analyze the binding profiles of KDM6A, H3K27me3, and H3K4me3 during differentiation in female and male ES cells. Additionally, ChiP-chip of KDM6A binding in control treated and siRNA treated ES cells is presented.
2013-03-22 | E-GEOD-45390 | biostudies-arrayexpress
Project description:Histone chaperones affect chromatin structure and gene expression through interaction with histones and RNA polymerase II (PolII). Here, we report that the histone chaperone Spt6 counteracts H3K27me3, an epigenetic mark deposited by the Polycomb Repressive Complex 2 (PRC2) and associated with transcriptional repression. We found that Spt6 is required for proper engagement and function of the H3K27 demethylase KDM6A (UTX) on muscle genes and regulates muscle gene expression and cell differentiation. ChIP-Seq experiments revealed an extensive genome-wide overlap of Spt6, PolII and KDM6A at transcribed regions that are devoid of H3K27me3. Mammalian cells and zebrafish embryos with reduced Spt6 display increased H3K27me3 and diminished expression of the master regulator MyoD, resulting in myogenic differentiation defects. As a confirmation for an antagonistic relationship between Spt6 and H3K27me3, inhibition of PRC2 permits MyoD re-expression in myogenic cells with reduced Spt6. Our data indicate that, through cooperation with PolII and KDM6A, Spt6 orchestrates removal of H3K27me3, thus effectively controlling developmental gene expression and cell differentiation. Examination of Spt6 and KDM6A levels in a skeletal muscle cells at various developmental stages
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Project description:The discovery of the first histone demethylase in 2004 (LSD1/KDM1) opened new avenues for the understanding of how histone methylation impacts cellular functions. A great number of histone demethylases have been identified since, which are potentially linked to gene regulation as well as to stem cell self-renewal and differentiation. KDM6A/UTY and KDM6B/JMJD3 are both H3K27me3/2-specific histone demethylases, which are known to play a central role in regulation of posterior development, by regulating HOX gene expression. So far nothing is known about the role of histone lysine demethylases (KDMs) during early hematopoiesis. We are studying the role of KDM6A and KDM6B on self-renewal, global gene expression and on local and global chromatin states in embryonic stem cells (ESCs) and during differentiation. In order to completely abrogate KDM6 demethylase activity in ESCs we employed a specific inhibitor (GSK-J4, Kruidenier et al. 2012). Treatment of ESCs with GSK-J4 had no effect on viability and proliferation . However, ESC differentiation in the presence of GSK-J4 was completely abrogated. In conclusion we show that ESC differentiation is completely blockend in the absence of any H3K27 demethylase activity. We used microarrays to detail the global gene expression program of genes which are differentially expressed during the early differentiation of ESC derived embryoid bodies (EBs) in the presence of GSK-J4 (KDM6 Inhibitor). ESCs (R1) have been cultured and differentiated in the presence of GSK-J4 a KDM6 specific inhibitor.
2016-03-11 | E-GEOD-49886 | biostudies-arrayexpress
Project description:As a histone hallmark for transcription repression, Histone H3 lysine 27 trimethylation (H3K27me3) plays important roles in mammalian embryo development and induced pluripotent stem cells (iPSCs) generation. However, the expression profile and roles of H3K27me3 in bovine somatic cell nuclear transfer (SCNT) reprogramming remain poorly understood. In this study, we find SCNT embryos exhibit global hypermethylation of H3K27me3 from two-cell to eight-cell stage and its removal by ectopically expressed H3K27me3 demethylase-KDM6A could greatly improves SCNT efficiency. To illuminate the mechanism of improving SCNT reprogramming efficiency of KDM6A overexpression, we performed RNA sequencing of transcripts in SCNT morula with or without KDM6A overexpression. RNA-seq reveal that KDM6A overexpression could enhance transcription of genes mainly involved cell adhesion and cellular metabolism process, as well as X-linked genes. We first provides the transcriptome data of bovine SCNT morula with or without KDM6A overexpression. Meanwhile, we compared the differences of transcriptome between SCNT eight-cell embryos and morula. Our study provide a more promising approach to improving the efficiency of SCNT reprogramming and contribute to understanding the mechanism of first cell fate determine during embryo development in bovine.
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Project description:Mammary ducts and alveoli are composed of basal and luminal cells, with the fate and differentiation of secreting cells being controlled by hormones through specific transcription factors. This study establishes the essential role of the histone H3 lysine 27 trimethylation (H3K27me3) demethylase KDM6A (UTX) in a balanced basal and luminal cell compartment. Disproportionate formation of basal cells in the absence of KDM6A resulted in disorganized mammary ducts and alveoli and lactation failure. Mutant luminal progenitors lost their distinctive transcription factor expression pattern and acquired basal characteristics leading to a preferential expansion of this lineage. The structure of mammospheres obtained from mutant progenitors suggested they were derived from basal progenitors. The genomic H3K27me3 landscape was unaltered in the absence of KDM6A suggesting demethylase-independent mechanisms. In support of this, mammary tissue developed normally in mice expressing a catalytically inactive KDM6A. This study demonstrated that mammary luminal progenitor cells rely on UTX to stably maintain their identity and thereby establish a balance of basal and luminal cells required for a functional mammary gland.
2016-06-06 | GSE77586 | GEO
Project description:Kdm6a is an X-linked histone demethylase that activates gene expression via removal of the repressive methylation mark at histone H3 lysine 27 (H3K27). In humans, KDM6A mutations cause Kabuki syndrome, a disorder characterized by intellectual disability and motor coordination deficits. To assess the role of Kdm6a in brain development and behavior, we generated a neuron-specific Kdm6a deficient mouse model using Cre-LoxP recombination. The mutant mice exhibited an adult-onset deficit in motor coordination. We then performed RNA-seq analysis to determine the mis-regulated genes that are listed in this dataset.
2017-05-06 | GSE81251 | GEO