Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243849 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1220080.fastq.gz | Fastqsanger.gz | |||
| SRR1220081.fastq.gz | Fastqsanger.gz | |||
| SRR1220082.fastq.gz | Fastqsanger.gz | |||
| SRR1220083.fastq.gz | Fastqsanger.gz | |||
| SRR1220084.fastq.gz | Fastqsanger.gz |
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Project description:The correlation between DNA methylation and a subset of histone post-translational modifications (positive and negative) has hinted at an underlying regulatory crosstalk between histone marks and DNA methylation in patterning the human DNA methylome, an idea further supported by corresponding alterations to both histone marks and DNA methylation during malignant transformation. This study investigated the framework by which histone marks influence DNA methylation at a genome-wide level. Using RNAi in a pluripotent human embryonic carcinoma cell line we depleted essential components of the MLL/COMPASS, polycomb repressive complex 2 (PRC2), and PRC1 histone modifying complexes that establish, respectively, the post-translational modifications H3K4me3, H3K27me3, and H2AK119ub, and assayed the impact of the subsequent depletion of these marks on the DNA methylome. Absence of H2AK119ub resulted predominantly in hypomethylation across the genome. Depletion of H3K4me3 and, surprisingly, H3K27me3 caused CpG island hypermethylation at a subset of loci. Intriguingly, many promoters were co-regulated by all three histone marks, becoming hypermethylated with loss of H3K4me3 or H3K27me3 and hypomethylated with depletion of H2AK119ub, and many of these co-regulated loci were among those commonly targeted for aberrant hypermethylation in cancer. Taken together, our results elucidate novel roles for polycomb and MLL/COMPASS in regulating DNA methylation and define targets of this regulation.
| S-EPMC4171634 | biostudies-literature
Project description:The association of DNA CpG methylation (or its absence) with occupancy of histone post translational modifications has hinted at an underlying crosstalk between histone marks and DNA methylation in patterning the human methylome, an idea supported by corresponding alterations to both histone marks and DNA methylation during malignant transformation. This study investigated the framework by which histone marks influence DNA methylation. Using RNAi in a human pluripotent embryonic carcinoma cell line we depleted essential components of the histone modifying complexes that establish the posttranslational modifications H3K4me3, H3K27me3, and H2AK119ub, and we assayed the impact of the subsequent loss of these marks on the DNA methylome. Absence of H2AK119ub resulted predominantly in hypomethylation across the genome. Removal of H3K4me3 or, surprisingly, H3K27me3 caused CpG island hypermethylation at a subset of loci. Intriguingly, many promoters were co-regulated by all three histone marks, becoming hypermethylated with loss of H3K4me3 or H3K27me3 and becoming hypomethylated with depletion of H2AK119ub, and many of these co-regulated loci were among those that are commonly, aberrantly hypermethylated in cancer.
2014-07-14 | GSE56535 | GEO
Project description:The association of DNA CpG methylation (or its absence) with occupancy of histone post translational modifications has hinted at an underlying crosstalk between histone marks and DNA methylation in patterning the human methylome, an idea supported by corresponding alterations to both histone marks and DNA methylation during malignant transformation. This study investigated the framework by which histone marks influence DNA methylation. Using RNAi in a human pluripotent embryonic carcinoma cell line we depleted essential components of the histone modifying complexes that establish the posttranslational modifications H3K4me3, H3K27me3, and H2AK119ub, and we assayed the impact of the subsequent loss of these marks on the DNA methylome. Absence of H2AK119ub resulted predominantly in hypomethylation across the genome. Removal of H3K4me3 or, surprisingly, H3K27me3 caused CpG island hypermethylation at a subset of loci. Intriguingly, many promoters were co-regulated by all three histone marks, becoming hypermethylated with loss of H3K4me3 or H3K27me3 and becoming hypomethylated with depletion of H2AK119ub, and many of these co-regulated loci were among those that are commonly, aberrantly hypermethylated in cancer.
2014-07-14 | GSE56538 | GEO
Project description:An epigenetic mark of polycomb response elements implemented by Trx/MLL/COMPASS
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Project description:This SuperSeries is composed of the SubSeries listed below.
2014-07-14 | GSE56539 | GEO
Project description:Methylation of lysine 4 at histone H3 (H3K4) at promoters is tightly linked to transcriptional regulation in human cells. At least six different COMPASS-like multi-subunit (SET1/MLL) complexes have been described that contain methyltransferase activity towards H3K4, but a comprehensive and quantitative analysis of these SET1/MLL complexes is lacking. We applied label-free quantitative mass spectrometry to determine the subunit composition and stoichiometry of the human SET1/MLL complexes. Peptides were applied to online nanoLC-MS/MS, using a 120 min acetonitrile gradient (5.6 - 76%). Mass spectra were recorded on an LTQ-Orbitrap-Velos mass spectrometer (Thermo) selecting the 15 most intense precursor ions of every full scan for fragmentation. Raw data were analyzed using MaxQuant 1.3.0.5, with label-free quantification (LFQ), match between runs (between triplicates) and the iBAQ algorithm enabled. MaxQuant default settings were used for peptide identification; Enzyme: Trypsin/P, MS tolerance (FTMS): 6 ppm, max missed cleavages: 2, max charge: 7, MS/MS tolerance (ITMS): 0.5 Da, Peptide FDR: 0.01 and Protein FDR: 0.01. Normalized mass spectrometric intensities (LFQ intensities) were compared between the GFP-tagged and control sample, using an adapted permutation-based false discovery rate (FDR) t-test in Perseus (MaxQuant package).
2013-09-13 | PXD000172 | Pride
Project description:In Drosophila, Polycomb Response Elements (PREs) are identified as genomic sequences allowing the maintenance of transcriptional repression in the absence of the initiating signal. Although PREs in Drosophila are well characterized, the existence of mammalian PRE-like elements remains debated. Accumulating evidence supports a model in which CpG islands function to recruit Polycomb-Group complexes (PcG), however, it is not evident which subclasses of CpG islands serve as PREs. Trithorax (Trx), which is required for positive regulation of gene expression in Drosophila, is known to co-bind Drosophila PREs where it is thought to antagonize polycomb-dependent silencing of nearby genes. Here, we demonstrate the existence of Trx-dependent H3K4 dimethylation loci that specifically mark Drosophila PREs and are required for the maintenance of expression of the nearby genes. Similarly, in human cells, we find ~ 3000 MLL1 (human Trx homologue)-dependent H3K4 dimethylation loci, which correlate strongly with CpG island density. In the absence of MLL1 and H3K4 dimethylation at these loci, there is an increase in H3K27 trimethylation levels, suggesting these sites can recruit Polycomb Repressive Complex 2 (PRC2). By inhibiting PRC2-dependent silencing in the absence of MLL1, we establish that a balance exists between MLL1 and PRC2, and their respective capacity to maintain or repress transcription. Thus, by investigating a conserved function between Trx and MLL1, we provide rules for the identification of CpG island subclasses serving as PRE-like sequences within the human genome. To examine changes in histone-modification profiles and gene expression after depletion of Trx in Drosophila S2 cells, and MLL1 in human HCT116 cells. We also treated MLL1-NULL HCT116 cells with GSK126 (5uM) for 4 days and measured changes in gene expression.
2016-07-26 | E-GEOD-81795 | biostudies-arrayexpress
Project description:Impact of human MLL/COMPASS and Polycomb complexes on the DNA methylome [expression array]
| PRJNA243852 | ENA
Project description:Impact of human MLL/COMPASS and Polycomb complexes on the DNA methylome [MBD-seq]
| PRJNA243850 | ENA
Project description:The evolutionally conserved COMPASS complexes are responsible for the catalyzation of H3K4 methylations. Recently, three types of COMPASS complexes which contains histone methyltransferases ATX1/2, ATX3, or ATX4/5 were identified in Arabidopsis. Here, we report the ATX proteins are essential for the survival of Arabidopsis. By RNA-seq and chromatin immunoprecipitation (ChIP-seq) analysis, we found ATX1/2-, ATX3-, and ATX4/5-containing COMPASS complex redundantly regulate gene expression and H3K4me3 modifications. In addition to the developmental-related genes, we found the expression of DNA methylation-related genes were also regulated by the COMPASS complexes. The transcript and H3K4me3 levels at the RdDM pathway genes (NRPE1, DCL3, IDN2, FDM2) and at the DNA demethylase encoding genes (ROS1, DML2, DML3) were down-regulated in atx1/2/4/5 mutants. Via bisulfate sequencing, we found the atx1/2/4/5 showed hypermethylation at CG and CHG contexts whereas the hypomethylation at CHH contexts. By comparing the differentially methylated regions (DMRs) in atx1/2/4/5 with that in ros1;dml2;dml3 (rdd) and in nrpe1, a large part of overlapping DMRs were identified. Based on these results and other findings, we propose that the hypermethylation in CG and CHG is partially caused by the down-regulation of ROS1/DML2/DML3, and the hypomethylation in CHH is mainly caused by the down-regulation of NRPE1. Furthermore, we revealed that the COMPASS complexes also play a redundant role in regulating the transcription of transposable elements (TEs). This study extends our knowledge about the function of COMPASS in plant development and illustrate the important roles for COMPASS complexes in the regulation of DNA methylation and TEs transcription.
2022-11-14 | GSE206685 | GEO