Project description:PcG protein complex PRC2 is a methyltransferase specific for histone H3 lysine27, and H3K27me3 is essential for stable transcription silencing. Here we have determined genomic distributions of H3K27me3, H3K27ac, and H3K4me1 in cultured Drosophila E(z) temperature sensitive cells at 25°C and 31°C where E(z) is largely inactivated by hybridization of ChIP products with tiling microarrays. Genomic distributions of H3K27me3, H3K27ac, and H3K4me1 in cultured Drosophila E(z) temperature sensitive cells (EZ2-2) at 25°C and 31°C where E(z) is largely inactivated by hybridization of ChIP products with tiling microarrays
Project description:PcG protein complex PRC2 is a methyltransferase specific for histone H3 lysine27, and H3K27me3 is essential for stable transcription silencing. Here we have determined genomic distributions of H3K27me3, H3K27ac, and H3K4me1 in cultured Drosophila E(z) temperature sensitive cells at 25°C and 31°C where E(z) is largely inactivated by hybridization of ChIP products with tiling microarrays.
Project description:Mono-methylation of histone H3 on lysine 4 (H3K4me1) and acetylation of histone H3 on lysine 27 (H3K27ac) are histone modifications that are highly enriched over the body of actively transcribed genes and enhancers. Although in yeast all H3K4 methylation patterns including H3K4me1 are implemented by Set1/COMPASS, there are three classes of COMPASS-like complexes in Drosophila that could carry out H3K4me1 on enhancers: dSet1, Trithorax and Trithorax-related (Trr). Here, we report that Trr, the Drosophila homolog of mammalian Mll3/4, can function as a major H3K4 mono-methyltransferase on enhancers in vivo. Loss of Trr results in a global decrease of H3K4me1 and H3K27ac in various tissues. Assays with the cut wing margin enhancer imply a functional role for Trr in enhancer-mediated processes. A genome-wide analysis demonstrates that Trr is required for H3K4me1 and H3K27ac on chromatin signatures that resemble the histone modification patterns described for enhancers. Since Trr and mammalian Mll3/4 complexes are distinguished by bearing a unique subunit, the H3K27 demethylase UTX, we propose a model in which the H3K4 mono-methyltransferase Trr, and the H3K27 demethylase, UTX, cooperate to regulate the transition from inactive/poised to active enhancers. ChIP-seq of Trr, LPT, UTX in Drosophila S2 Cells. ChIP-seq of H3K4me1, H3K4me3, H3K27ac, H3K27me3 in WT and Trr knock-down Drosophila S2 cells. ChIP-seq of H3K4me1, H3K27me3 in LPT knock-down Drosophila S2 cells. ChIP-seq of LPT and UTX in Trr knock-down Drosophila S2 cells. ChIP-seq of H3K4me1 and H3K27me3 in MLL1(+/+), MLL1(-/-), MLL3(+/+), and MLL3(-/-) Mouse Embryonic Fibroblasts (MEFs).
Project description:WS234 cells are an immortalized human cell line. Here we have explored the distribution of histone marks (H3K27me3, H3K27ac, H3K4me3, H3K4me1, and H3K9me3) across the genome in proliferative conditions.
Project description:We report the distribution of histone H3K4me1 and H3K27ac within the genome of mouse embryonic midbrain. We prepared the chromatin from 11 dpc embryonic midbrain and made chromatin precipitation with antibody against H3K4me1 and H3K27ac (rabbit polyclonal antibody). High-throughput sequencing applied for the ChIP analysis revealed the differential distribution of modified histone within developing midbrain. ChIP analysis of mouse 11 dpc embryonic midbrain and forelimb buds against anti-H3K4me1 and H3K27ac antibody.