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:RBP2 (JARID1A/RBBP2) enrichment at proximal promoter regions in differentiating promonocytic U937 cells and in the osteosarcoma SAOS-2 cells Keywords: differentiation treatment, ChIP-on-chip analysis
Project description:RBP2 (JARID1A/RBBP2) enrichment at proximal promoter regions in differentiating promonocytic U937 cells and in the osteosarcoma SAOS-2 cells Keywords: differentiation treatment, ChIP-on-chip analysis We sought to determine transcriptional regulation by RBP2 genome-wide by using location analysis. We describe that RBP2 target genes are separated into two functionally distinct classes: differentiation independent and differentiation dependent genes.Three condition experiment, U937 cells treated with 100 nM 12-O-tetradeconoyl-phorbol 13-acetate (TPA) (Sigma) for two different time points (27 hrs and 96 hrs) and untreated (0 hrs time point or no TPA treatment). In addition, processed data for the unrelated SAOS-2 cells are included. Biological replicates: threechromatin immunoprecipitations (ChIP) performed independently in parallel
Project description:OCI-AML3 Acute myeloid leukemia cell line was used for ChIP-sequencing profiling of H3K4me3, H3K4me1, H3K9ac and H3K27ac histone post-translational modifications to identify active promoter and enhancer regions.
Project description:Tenderness is one of the most important properties of meat quality, which is influenced by genetic and environmental factors. As an intensively studied epigenetic marker, histone methylation, occurring on arginine and lysine residues, has pivotal regulatory functions on gene expression. To examine whether histone methylation involves in beef tenderness variation, we analyzed the transcriptome and H3K4me3 enrichment profiles of muscle strips obtained from the longissimus dorsi (LD) of Angus steers previously classify to the tender or tough group. We first plotted a global bovine H3K4me3 map on chromosomes and called peak-enriched regions and genes. We found that majorities of H3K4me3 on genes were occupying the first intron and intergenic regions and its maps displayed similar patterns in tender and tough groups, with high H3K4me3 enrichment surrounding the transcription start site (TSS). We also explored the relationship of H3K4me3 and gene expression. The results showed that H3K4me3 enrichment is highly positively correlated with gene expression across the whole genome. Cluster analysis results confirmed the relationship of H3K4me3 enrichment and gene expression. By using a pathway-based approach in genes with H3K4me3 enrichment in promoter regions from the tender cluster, we revealed that those genes involved in the development of different tissues–connective tissue, skeletal and muscular system and functional tissues–; while in tough group those genes engaged in cell death, lipid metabolism and small molecule biochemistry. The results from this study provide a deep insight into understanding of the mechanisms of epigenetic regulations in meat quality and beef tenderness.
Project description:Stress-induced mental disorders, including depression and anxiety disorders, constitute a global issue in contemporary society due to treatment complexity and the diversity of manifestations. Understanding the molecular mechanisms of these disorders presents a significant challenge for neurobiology. We investigated the effects of social defeat stress (SDS) of varying durations (10 and 30 days) on behavioral patterns and the H3K4me3 landscape in the prefrontal cortex of C57BL/6 mice. Furthermore, we compared these data with previously published H3K4me3 landscape data obtained after 15 days of SDS and transcriptomic data collected after 10, 15, and 30 days. We discovered that a 30-day period of stress results in more pronounced depressive-like behavior. SDS induces slight alterations in the H3K4me3 density across numerous nucleosomal peaks. The analysis of differential enrichment peaks of H3K4me3 in promoter regions following varying durations of SDS revealed that the aggregation of multiple H3K4me3 nucleosome peaks in the promoter region functions as a QR code, likely affecting the promoter's state regarding the accessibility of transcription factors. Furthermore, we identified a cluster of genes in the promoter regions exhibiting differential enrichment peaks of H3K4me3 following SDS of any duration. This cluster includes genes encoding transcription factors such as Mef2c and Nr4a3, as well as postsynaptic density proteins (Shank2, Shank1, and Gria2), which are associated with stress sensitivity and the onset of depression; their protein products are involved in synaptic transmission and signal transduction mechanisms. The comparison of ChIP-seq and RNA-seq data following varying durations of SDS stress enabled a deeper insight intothe dynamics of SDS-induced changes. Together, these findings understanding of the molecular mechanisms of SDS in the prefrontal cortex.
Project description:De novo ASXL1 mutations are found in patients with Bohring-Opitz syndrome (BOS), a disease with severe developmental defects and early childhood fatality. The underlying pathologic mechanisms remain largely unknown. Using Asxl1-targeted murine models, we found that Asxl1 global loss or conditional deletion in osteoblasts and their progenitors in mice leads to significant bone loss and markedly decreased numbers of marrow mesenchymal stem/progenitor cells (MSPCs) compared with wild-type (WT) littermates. Asxl1 null MSPCs display impaired self-renewal and skewed differentiation from osteoblasts towards adipocytes. ChIP-seq data identified that ASXL1 and H3K4me3 co-occupy the promoter regions of genes critical for MSPC self-renewal. Loss of Asxl1 diminished the genome enrichment of H3K4me3. Combined analysis of RNA-seq and ChIP-seq data revealed that Asxl1 loss in MSPCs altered the expression of ASXL1/H3K4me3 target genes controlling self-renewal/lineage commitment. Our study unveil a pivotal role of ASXL1 in H3K4me3-associated bone homeostasis
Project description:We have investigated the genome-wide occupancy of Sas3p by ChIP-Chip, using tiled microarrays. Using this technique, it has been described that H3K14 and H3K9 acetylation is enriched at promoter regions and transcriptional start sites of active genes. Considering that Sas3p is a HAT whose main target in vitro is H3K14 we expected to detect Sas3 binding largely to promoter regions of genes. Surprisingly, we found that Sas3p is associated to the coding regions of genes, with a peak enrichment located) within the 5’ half of the ORF, and this enrichment drops substantially toward the 3’ region of the ORF. This result is very similar to that obtained for Yng1 genome-wide occupancy, also a component of the NuA3 complex, suggesting that this complex could be involved in transcriptional elongation, at least, in an initial step of the process.
Project description:Epigenome profiling has led to the paradigm that promoters of active genes are decorated with H3K4me3 and H3K9ac marks. Data revealed an extensively euchromatic epigenome with heterochromatin restricted to variant surface antigen gene families (VSA) and a number of genes hitherto unlinked to VSA. The vast majority of the genome shows an unexpected pattern of enrichment of H3K4me3 and H3K9ac at intergenic regions and depletion at genes. Chip-chip (and cDNA) from Plasmodium falciparum strain NF54 asexual blood stages with H3, H3K4me3, H3K9me3 and H3K9ac
Project description:Arabidopsis telomeric repeat binding factors (TRBs) can bind telomeric DNA sequences to protect telomeres from degradation. TRBs can also recruit Polycomb Repressive Complex 2 (PRC2) to deposit tri-methylation of H3 lysine 27 (H3K27me3) over certain target loci. Here, we demonstrate that TRBs also associate and colocalize with JUMONJI14 (JMJ14) and trigger H3K4me3 demethylation at some loci. The trb1/2/3 triple mutant and the jmj14-1 mutant show an increased level of H3K4me3 over TRB and JMJ14 binding sites, resulting in up-regulation of their target genes. Furthermore, tethering TRBs to the promoter region of genes with an artificial zinc finger (TRB-ZF) successfully triggers target gene silencing, as well as H3K27me3 deposition, and H3K4me3 removal. Interestingly, JMJ14 is predominantly recruited to ZF off-target sites with low levels of H3K4me3, which is accompanied with TRB-ZFs triggered H3K4me3 removal at these loci. These results suggest that TRB proteins coordinate PRC2 and JMJ14 activities to repress target genes via H3K27me3 deposition and H3K4me3 removal.