Changes in H3K4 methylation in KDM5A/JARID1A/RBP2 knockout cells.
Ontology highlight
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. Examination of histone methylation in the absence of histone demethylase RBP2
Project description:Here we report the identification of genomic regions of DNA bound by Dp1 in Drosophila S2R+ cells. Dp1 is a dimerization partner of several E2F transcription factors and is needed for E2F target promoter binding. We find that Dp1 binds the promoter regions of genes important for oxidative phosphorylation. This result is important since our data demonstrates that expression of several oxidative phosphorylation genes is down-regulated in dDP mutant Drosophila 3rd instar larval eye imaginal discs. These ChIP-seq results suggest that the mechanism by which dDP regulates expression of these genes is direct. In addition, we have confirmed a number of these Dp1 bound gene promoters by conventional Chromatin Immunoprecipitation. Examination of Dp1 bound regions of genomic DNA in S2R+ 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
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.
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.
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.
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.
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
Project description:RNA-sequencing analysis of RBP2 overexpressing MCF7 cell lines. RBP2 (also known as JARID1A), a member of the JARID1 family of histone H3 lysine K4 demethylases, has been considered to have an oncogenic potential in several cancer including breast cancer. Results provide insight into the transcriptional regulation of RBP2 in estrogen receptor positve breast cancer.
Project description:H3K4me3 enrichment at proximal promoter regions Keywords: ChIP-on-chip data We describe that RBP2 shows high correlation with the presence of H3K4me3. Biological replicates: chromatin immunoprecipitations were performed independently in parallel
Project description:Aberrations in epigenetic processes, such as histone methylation, can lead to cancer. Retinoblastoma Binding Protein 2 (RBP2)(also called JARID1A or KDM5A) can demethylate tri- and di-methylated lysine 4 in histone H3, which are epigenetic marks for transcriptionally active chromatin, whereas the MEN1 tumor suppressor promotes H3K4 methylation. Previous studies suggested that inhibition of RBP2 contributed to tumor suppression by pRB. Here we show RBP2 loss promotes cellular differentiation in vitro. We use mouse expression array 430 2.0 array to profile gene expression patterns of Rbp2f/f and Rbp2-/- ES cells in ES cell medium and after 6 days in ES cell medium without LIF.