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SRX12764411: GSM5653836: H3K27me2_ChIP-seq_mESC_WT; Drosophila melanogaster; Mus musculus; ChIP-Seq
1 ILLUMINA (Illumina NovaSeq 6000) run: 40.9M spots, 4.1G bases, 1.3Gb downloads

Submitted by: NCBI (GEO)
Study: H3K36 Dimethylation Shapes the Epigenetic Interaction Landscape by Directing Repressive Chromatin Modifications in Embryonic Stem Cells
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Epigenetic modifications on the chromatin do not occur in isolation. Chromatin associated proteins and their modification products form a highly interconnected network, and disturbing one component may rearrange the entire system. We see this increasingly clearly in epigenetically dysregulated cancers. It is important to understand the rules governing epigenetic interactions. Here, we use the mouse embryonic stem cell (mESC) model to describe in detail the relationships within the H3K27-H3K36-DNA methylation subnetwork. In particular, we focus on the major epigenetic re-organization caused by deletion of the histone 3 lysine 36 methyltransferase NSD1, which in mESCs deposits nearly all of the intergenic H3K36me2. Although disturbing the H3K27 and DNA methylation (DNAme) components also affects this network to a certain extent, the removal of H3K36me2 has the most drastic effect on the epigenetic landscape, resulting in full intergenic spread of H3K27me3 and a substantial decrease in DNAme. By profiling DNMT3A and CHH methylation (mCHH), we show that H3K36me2 loss upon Nsd1-KO leads to a massive re-distribution of DNMT3A and mCHH away from intergenic regions and towards active gene bodies, suggesting that DNAme reduction is at least in part caused by redistribution of de novo methylation. Additionally, we show that pervasive acetylation of H3K27 is regulated by the interplay of H3K36 and H3K27 methylation. Our analysis highlights the importance of H3K36me2 as a major determinant of the developmental epigenome and provides a framework for further consolidating our knowledge of epigenetic networks. Overall design: WGBS, RNA-seq, and ChIP-seq for histone H3 post-translational modifications in mouse embryonic stem cells (mESC).
Sample: H3K27me2_ChIP-seq_mESC_WT
SAMN22560439 • SRS10711490 • All experiments • All runs
Library:
Instrument: Illumina NovaSeq 6000
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: About 10 million cells per cell line were grown and directly crosslinked on the plate with 1% formaldehyde (Sigma) for 10 minutes at room temperature and the reaction was stopped using 125nM Glycine for 5 minutes. Fixed cell preparations were washed with ice-cold PBS, scraped off the plate, pelleted, washed twice again in ice-cold PBS, and flash frozen pellets stored at −80°C. Thawed pellets were resuspended in 500ul cell lysis buffer (5 mM PIPES-pH 8.5, 85 mM KCl, 1% (v/v) IGEPAL CA-630, 50 mM NaF, 1 mM PMSF, 1 mM Phenylarsine Oxide, 5 mM Sodium Orthovanadate, EDTA-free Protease Inhibitor tablet) and incubated 30 minutes on ice. Samples were centrifugated and pellets resuspended in 500ul of nuclei lysis buffer (50 mM Tris-HCl pH 8.0, 10 mM EDTA, 1% (w/v) SDS, 50 mM NaF, 1 mM PMSF, 1 mM Phenylarsine Oxide, 5 mM Sodium Orthovanadate and EDTA-free protease inhibitor tablet) and incubated 30 minutes on ice. Sonication of lysed nuclei was performed on a BioRuptor UCD-300 at max intensity for 60 cycles, 10 s on 20 s off, centrifuged every 15 cycles, chilled by 4°C water cooler. Samples were checked for sonication efficiency using the criteria of 150-500bp by gel electrophoresis of a reversed cross-linked and purified aliquot. After the sonication, the chromatin was diluted to reduce SDS level to 0.1% and concentrated using Nanosep 10k OMEGA (Pall). Before ChIP reaction 2% of sonicated Drosophila S2 cell chromatin was spiked-in the samples for quantification of total levels of histone mark after the sequencing. ChIP reaction for histone modifications was performed on a Diagenode SX-8G IP-Star Compact using Diagenode automated Ideal ChIP-seq Kit for Histones. Dynabeads Protein A (Invitrogen) were washed, then incubated with specific antibodies, 1.5 million cells of sonicated cell lysate, and protease inhibitors for 10 hr, followed by 20 min wash cycle using the provided wash buffers (Diagenode Immunoprecipitation Buffers, iDeal ChIP-seq kit for Histone). Reverse cross-linking took place on a heat block at 65°C for 4 hr. ChIP samples were then treated with 2ul RNase Cocktail at 65°C for 30 min followed by 2ul Proteinase K at 65°C for 30 min. Samples were then purified with QIAGEN MinElute PCR purification kit (QIAGEN) as per manufacturers' protocol. In parallel, input samples (chromatin from about 50,000 cells) were reverse cross-linked and DNA was isolated following the same protocol. KAPA Hyper Prep Kit
Experiment attributes:
GEO Accession: GSM5653836
Links:
Runs: 1 run, 40.9M spots, 4.1G bases, 1.3Gb
Run# of Spots# of BasesSizePublished
SRR1656228740,903,4054.1G1.3Gb2022-03-30

ID:
17365342

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