Project description:We report a map of H3K4me3 - an activiting expression histone modification in C6 rat glioma cells. The data was obtained using whole genome high throughput technology. The sequencing was performed on Solid 5500xl platform. Examination of H3K4me3 histone modification in C6 rat glioma cell line
Project description:Histone modification H3K27me3 profilings by the CUT&RUN method (Skene et al., 2017) were performed using embryonic callus and non-embryonic callus of Picea abies to identify genes related to somatic embryogenesis capacity.
Project description:Heterochromatin contains repressively modified histones and replicates late in S phase of the cell cycle. Besides the shortage in replication origins, little is known about replication timing regulation in silenced regions. In Drosophila polytene cells, late replication results in under-replication and decreased DNA copy number in heterochromatic regions of the genome. The Suppressor of Under-replication (SUUR) protein controls this feature â in its absence the DNA polytenization level in most silenced regions is restored, however the repressive histone marks are lost. We hypothesized that SUUR regulates the re-establishment of repressive histone pattern during replication which results in delayed replication completion of heterochromatin. Measuring DNA copy number in mutants with disrupted repressive pathways, we found that under-replication is directly linked to repressive histone marks supply. DamID-seq and ChIP-seq experiments revealed that SuUR mutation does not affect the establishment of heterochromatin domains. Here, we identified a novel SUUR protein interaction (CG12018) that supports SUUR association with replication complex. SUUR loads onto replication forks shortly after the origin firing and participates in chromatin maintenance rather than its establishment. Thus, our findings provide comprehensive evidence that late replication in Drosophila is caused by the time-consuming process of replication-coupled repressive chromatin renewal. Examination of H3K27me3 histone modification in 3 cell types in presence or absence of SuUR mutation.
Project description:To investigate the impact of histone variants and modification on gene regulation, we report high-throughput profiles of six histone markers, H2A.Z, H3K4me2, H3K9me3, H3K27me3, H3K27ac, and H3K36me3, by ChIP-Seq in T-47D breast cancer cells. Libraries were sequenced with the Illumina HiSeq 2000 analyzer for 50 bp paired-end reads and over 20 million uniquely aligned reads were collected for each histone marker. To examine the impact of histone modification on gene expression regulation in T-47D cells.
Project description:The perturbations of ER homeostasis lead to the development of a condition referred to as ER stress. However, the repressive trimethylation on histone H3 lysine 27 (H3k27me3) under ER stress remains largely elusive. Here, we identify a critical role for H3k27me3 to impact the expression of Crytochrome 1 (Cry1). To examine the effect of ER stress on histone modification, MEFs were treated with vehicle 2μg/ml tunicamycin for 6 h. The cell lysate were collected and ChIP-seq assays were performed with the primary H3k27me3 or H3k4me3 antibody. When compared to the Vehicle group, the tunicamycin treatment reduced the 23,008 H3k27me3 peaks. In line with the roles of H3k27me3 in the regulation of gene transcriptions, annotation of the peak in genomic positions to the cloest genes indicated that many peaks were positioned after the transcription start site. Cry1 is one of the most regulated genes. However, the tunicamycin treatment slightly reduced H3k4me3 modification in MEFs. There are only 3109 peaks were decreased by the tunicamycin treatment. These data suggest ER stress selectively regulated H3k27me3 modification in the hisone 3 and reactivate Cry1 gene expression in MEFs.
Project description:BAF complex is one major group of chromatin remodeling factors in mammals. However, how BAF regulated nucleosomes and other histone modifications is not clear. Here we delete BAF250a, a major component in esBAF to study the nucleosome and histone changes in ESCs. We find that deletion of BAF250a leads to nucleosome occupancy increase in TSS regions and non-pioneer transcription factor binding sites. BAF250a deletion also cause overall decrease of H3K27me3 modification. Collectively, these results reveals how BAF complex coordinates nucleosome, histone modification to control ESC function. Sample 1-4: Nucleosome profiles in WT and BAF250a KO ESCs. Sample 5-10: profiling of H3K4me3 and H3K27me3 in WT and BAF250 KO ESCs.
Project description:The histone modification H3K27me3 is representative of silenced regions of the genome. Changes between the normal and cancer state were investigated. Three PrEC samples, a normal cell line. Four LNCaP sample, a cancer cell line. Technical replicates.