Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3184720_1.fastq.gz | Fastqsanger.gz | |||
| ERR3184720_2.fastq.gz | Fastqsanger.gz | |||
| ERR3184730_1.fastq.gz | Fastqsanger.gz | |||
| ERR3184730_2.fastq.gz | Fastqsanger.gz | |||
| ERR3184740_1.fastq.gz | Fastqsanger.gz |
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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:Recent studies indicate that thousands of genes are expressed from bidirectional promoters (BDPs). Gene regulation at BDPs is poorly understood, in particular how the cell is able to regulate them differently. Here we investigate the effect of histone Modifications in BDP regulation. In this study, we model the gene activity using different gene expression assays, such as RNA-Seq, GRO-cap, and CAGE around the BDP transcription start sites (TSSs) using different histone modifications in various cell types. We develop a new statistical approach that links histone modifications to gene expression at BDPs. It improves over previous methods, because it is able to capture spatial dependencies of histone modifications along a promoter and leads to more interpretable results. We predict a general histone code that is independent of transcript orientation, cell type, and promoter configuration. The histone code at BDPs reveals that promoters are regulated unidirectionally, such that the majority of histone marks associated with gene expression occur downstream of the gene's TSS. By contrasting associations of histone marks with steady-state levels of capped RNAs in CAGE and nascent capped RNAs in GRO-cap, we show which histone marks have a preference for initiating polymerases and actively elongating polymerases. Using single-cell data we show that the bidirectional histone signal of activating marks is often due averaging of a heterogeneous cell population. Our results have implications for other experiments where the relationship between histone modification and gene initiation or gene elongation is investigated on a genome-wide scale.
| EGAS00001001656 | EGA