Similar Datasets
Project description:We report the identification of 67 previously undescribed histone modifications, increasing the current number of known histone marks by about 70%. We further investigated one of the marks, lysine crotonylation (Kcr), confirming that it represents an evolutionarily-conserved histone posttranslational modification. The unique structure and genomic localization of histone Kcr suggest that it is mechanistically and functionally different from histone lysine acetylation (Kac). Specifically, in both human somatic and mouse male germ cell genomes, histone Kcr marks either active promoters or potential enhancers. In male germinal cells immediately following meiosis, Kcr is enriched on sex chromosomes and specifically marks testis-specific genes, including a significant proportion of X-linked genes that escape sex chromosome inactivation in haploid cells. These results therefore dramatically extend the repertoire of histone PTM sites and designate Kcr as a specific mark of active sex chromosome-linked genes in postmeiotic male germ cells. 2 histone marks (pan-lysine acetylation and pan-lysine crotonylation) were studied in 1 human cell type and 2 mouse cell types using ChIP-Seq. Input was sequenced for each cell type as a control. Pan-anti_Kac and pan-anti_Kcr antibodies were custom developed with PTM BioLab, Co., Ltd (Chicago, IL).
2011-10-06 | E-GEOD-32663 | biostudies-arrayexpress
Project description:This experiment used ChIP-seq technology to create a genome-wide profile of histone marks in normal human pancreatic islets. In the current work we analyzed two histone marks associated with gene expression (H3K4me3, H3K4me1) and marks associated with gene repression(H3K27me3). Each mark was anayzed using samples obtained from four donors (n=4). Chromatin Immunoprecipitations (ChIPs) for histone marks were performed using specific anti-histone antibodies. Enrichment of each sample was calulated with respect to its individual input using qPCR. Samples were sequenced with Solexa and sequenced DNA from both Input (n=4) and ChIP (n = 4) samples were aligned to the NCBI Genome Build 36.1 Ð Hg18 to determine regions that were enriched for binding by modified histones.
2010-02-18 | E-MTAB-189 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE38410: Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation (mRNA) GSE38442: Independence of Repressive Histone Marks and Chromatin Compaction during Senescent Heterochromatic Layer Formation (ChIP-Seq) Refer to individual Series
2012-07-08 | E-GEOD-38448 | biostudies-arrayexpress
Project description:Epigenetic states defined by chromatin can be maintained through mitotic cell division. However, it remains unknown how histone-based information is transmitted. Here we combine nascent chromatin capture (NCC) and triple-SILAC labelling to track histone modifications and histone variants during DNA replication and across the cell cycle. We show that post-translational modifications (PTMs) are transmitted with parental histones to newly replicated DNA. Di- and tri-methylation marks are diluted two-fold upon DNA replication, as a consequence of new histone deposition. Importantly, within one cell cycle all PTMs are restored. In general, new histones are modified to mirror the parental histones. However, H3K9me3 and H3K27me3 are propagated by continuous modification of parental and new histones, because the establishment of these marks extends over several cell generations. Together, our results reveal how histone marks propagate and demonstrate that chromatin states oscillate within the cell cycle.
2015-03-30 | PXD001980 | Pride
Project description:Epigenetic regulation is a dynamic and reversible process that controls gene expression. Abnormal function results in downregulation or upregulation of pathways leading to diseases, such as cancer. The enzymes that establish and maintain epigenetic marks, such as histone methyltransferases (HMTs), are therapeutic targets as their and, importantly, the epigenetic modifications are reversible. Noteworthy, HMTs, as the other epigenetic enzymes and readers, form together multiprotein complexes that in concert regulate histone marks. To probe the epigenetic protein complexes in a biological system, we developed a reliable chemical biology high-content imaging strategy to screen compound libraries on multiple histone marks inside cells simultaneously. The advantage is double: (1) it identifies directly a drug that is active in cells on a specific histone mark and (2) it reveals the crosstalk between the epigenetic marks. By this approach, we identified that compound 4, a published CARM1 (PRMT4) inhibitor, inhibits both histone mark H3R2me2a (regulated by CARM1) and H3K79me2 (regulated by DOT1L) pointing out a synergistic interaction between the two HMTs. The results obtained by the screening assay were validated by mass spectrometry and other techniques confirming the crosstalk between the two marks and HMTs. Prompted by the interaction between CARM1 and DOT1L we combined compound 4 and DOT1L inhibitor EPZ-5676 resulting in a stronger cell proliferation inhibition and apoptosis, indicating that our approach provides also a novel strategy to identify effective synergistic drug combinations for cancer therapy.
2022-05-19 | PXD022873 | Pride
Project description:Genome-wide occupancy of biotinylated Jmjd2b, Jmjd2c from mESCs, as well as occupancy of selected factors and histone marks from wild-type mESCs, Anti-GFP KD, Jmj2b KD and Jmjd2c KD mESCs genome To identify genome-wide binding target sites of Jmjd2b and Jmjd2c in the mESCs genome, and genome-wide binding sites for selected factors and histone marks from Anti-GFP KD, Jmjd2b KD and Jmjd2c KD mESCs
2013-12-01 | E-GEOD-43229 | biostudies-arrayexpress