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Changes in H3K4 methylation in KDM5A/JARID1A/RBP2 knockout cells.

ABSTRACT: We sought to determine H3K4me3 distribution in mouse embryonic stem (ES) cells deficient for RBP2 compared with wild-type cells. RBP2 modifies methylated lysine residues on histone tails. As a result of this analysis, we identified genomic regions with changed H3K4me3 status and described these in gene ontology (GO) categories.

ORGANISM(S): Mus musculus

PROVIDER: GSE28348 | GEO | 2015/08/12

SECONDARY ACCESSION(S): PRJNA139457

REPOSITORIES: GEO

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Changes in H3K4 methylation in KDM5A/JARID1A/RBP2 knockout cells.

Project description:We sought to determine H3K4me3 distribution in mouse embryonic stem (ES) cells deficient for RBP2 compared with wild-type cells. RBP2 modifies methylated lysine residues on histone tails. As a result of this analysis, we identified genomic regions with changed H3K4me3 status and described these in gene ontology (GO) categories. Examination of histone methylation in the absence of histone demethylase RBP2

2015-08-12 | E-GEOD-28348 | biostudies-arrayexpress

Genome-wide maps of KDM5A/JARID1A/RBP2 and its isoforms in differentiated U937 cells

Project description:We report the identification of genomic regions bound by RBP2 isoforms and define the functional categories that these regions represent. RBP2 modifies methylated lysine residues on histone tails. We found that RBP2 large isoform containing the recognition module for histone H3K4me3 and RBP2 small isoform lacking this module bind to to different regions in the human genome. Importantly, isoform-specific regions and overlapping regions belong to genes with different molecular functions. For example, chromatin binding and transcription factor binding functions can be ascribed to gene targets of RBP2 small isoform but not of RBP2 large isoform. By comparing gene sets generated for all isoforms and RBP2 large isoform, we can define if the small isoform is specifically recruited to genomic regions dispaying certain signatures, such as transcription start sites, CpG-rich regions, transcriptional activity and transcription factor binding.

2015-03-23 | GSE28323 | GEO

Genome-wide maps of KDM5A/JARID1A/RBP2 in mouse ES cells.

Project description:We report the identification of genomic regions bound by KDM5A in mouse embryonic stem (ES) cells and define the functional categories that these regions represent. KDM5A modifies methylated lysine residues on histone tails. We developed anti-KDM5A antibodies and set to detect genomic regions enriched with these antibodies using cells with normal Kdm5a or cells from Kdm5a knockout mice as a control. We found high enrichment with the KDM5A antibodies in normal cells when compared with the genomic background. We found striking identity in the regions enriched with these antibodies in normal cells when compared with the total genomic DNA or with KDM5A ChIP assays from Kdm5a KO cells, showing that the antibodies are specific. Examination of target genes in ES cells

2012-10-04 | E-GEOD-28343 | biostudies-arrayexpress

Genome-wide maps of KDM5A/JARID1A/RBP2 in mouse ES cells.

2012-10-04 | GSE28343 | GEO

Genome-wide maps of KDM5A/JARID1A/RBP2 and JARID2/JMJ in HL-1 cardiomyocytes.

Project description:We report the identification of genomic regions bound by RBP2 and JARID2 in mouse cardiomyocytes. RBP2 generates methylated lysine 4 in histone H3. Consistent with previous data, RBP2 binds at the TSS regions. However, we found that overepresentation of gene ontologies (GO) for RBP2 targets in cardiomyocytes is drastically different from those in mouse embryonic stem (ES) cells. In cardiomyocytes, there is overepresentation of genes involved in heart morphogenesis and vasculogenesis. Strikingly, we found that location of JARID2, a factor critical for ES cell function, significantly overlaps with RBP2 location in cardiomyocytes.

2018-04-01 | GSE28341 | GEO

Genome-wide maps of KDM5A/JARID1A/RBP2 and KDM5B/JARID1B/PLU1 in estrogen treated MCF7 cells.

Project description:We report the identification of genomic regions bound by RBP2 in MCF7 (ER+) cells and the MCF7 cells that were treated with estradiol. RBP2 is recruited to TSS regions and shows preference for GC-rich regions. We find the regions differentially bound by RBP2 after estrogen treatment. These regions will be correlated with binding of ER, H2A.Z and high/low transcriptional activity. We also report genomic regions bound by RBP2 closest homolog, PLU1. PLU1 location does not overlap with RBP2 binding sites. In contrast to RBP2, PLU1 does not show very high enrichment at TSS. This suggests that these two histone demethylases are preferentially located in different regions.

2018-04-01 | GSE28337 | GEO

The Retinoblastoma Binding Protein RBP2 is an H3K4 demethylase

Project description:The roles of histone demethylase RBP2 in gene expression were assessed using gene expression profiling experiments with wild type and RBP2-/- primary MEFs. Several cytokine genes including SDF1 and Kit ligand were upregulated upon inactivation of RBP2. Keywords: mouse embryonic fibroblasts, gene expression profiling, microarray, Affymetrix Mouse Genome 430 2.0, cell type comparison

2007-02-22 | GSE6945 | GEO

Transcription profiling of mouse primary embryonic fibroblasts reveals the retinoblastoma binding protein RBP2 is an H3K4 demethylase

Project description:The roles of histone demethylase RBP2 in gene expression were assessed using gene expression profiling experiments with wild type and RBP2-/- primary MEFs. Several cytokine genes including SDF1 and Kit ligand were upregulated upon inactivation of RBP2. Experiment Overall Design: Total RNA were extracted from two independent lines of wild type and RBP2 primary MEFs at passage 3 and analyzed for gene expression profiles using Affymetrix platform.

2008-06-15 | E-GEOD-6945 | biostudies-arrayexpress

Maintenance of gene silencing by the coordinate action of the H3K9 methyltransferase G9a/KMT1C and the H3K4 demethylase Jarid1a/KDM5A.

Project description:Chromatin remodeling is essential for controlling the expression of genes during development. The histone-modifying enzyme G9a/KMT1C can act both as a coactivator and a corepressor of transcription. Here, we show that the dual function of G9a as a coactivator vs. a corepressor entails its association within two distinct protein complexes, one containing the coactivator Mediator and one containing the corepressor Jarid1a/KDM5A. Functionally, G9a is important in stabilizing the Mediator complex for gene activation, whereas its repressive function entails a coordinate action with the histone H3 lysine 4 (H3K4) demethylase Jarid1a for the maintenance of gene repression. The essential nature of cross-talk between the histone methyltransferase G9a and the demethylase Jarid1a is demonstrated on the embryonic E(y)-globin gene, where the concurrent introduction of repressive histone marks (dimethylated H3K9 and dimethylated H3K27) and removal of activating histone mark (trimethylated H3K4) is required for maintenance of gene silencing. Taken together with our previous demonstration of cross-talk between UTX and MLL2 to mediate activation of the adult ?(maj)-globin gene, these data suggest a model where "active" and "repressive" cross-talk between histone-modifying enzymes coexist on the same multigene locus and play a crucial role in the precise control of developmentally regulated gene expression.

| S-EPMC3503177 | biostudies-literature

Myogeneic differentiation in Rb1 or Kdm5a/Jarid1a/Rbp2 deficient mouse embryonic fibroblasts.

Project description:Cells lacking Rb1 are deficient in differentiation. Loss of Kdm5a rescues myogenic differentiation, as judged by appearance of morphologically normal myotubes that display expression of late markers of differentiation. In order to better understand how Kdm5a loss rescues differentiation, we induced mouse embryonic fibroblasts (MEFs) of different genotypes to undergo myogenic differentiation and analyzed gene expression changes in wild-type, Kdm5a-/-, Rb1-/- and Kdm5a-/-; Rb1-/- cells. Rb1-/- cells stained single nucleated, did not exhibit morphological changes and increased expression of the myogenic marker MYHC. Except for Rb1-/- cells, all other cells were undergoing successful convertion into aligned multinucleated myotubes and were MYHC-positive. We obtained purified populations of myotubes for the wild-type and Kdm5a-/-; Rb1-/- cells.

2015-08-12 | GSE53528 | GEO

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