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SRX12764399: GSM5653825: H3K27me3_ChIP-seq_mESC_WT_A1; Mus musculus; ChIP-Seq
1 ILLUMINA (Illumina HiSeq 4000) run: 29M spots, 8.7G bases, 3.4Gb downloads

Submitted by: NCBI (GEO)
Study: H3K36 Dimethylation Shapes the Epigenetic Interaction Landscape by Directing Repressive Chromatin Modifications in Embryonic Stem Cells
show Abstracthide Abstract
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: H3K27me3_ChIP-seq_mESC_WT_A1
SAMN22560422 • SRS10711479 • All experiments • All runs
Organism: Mus musculus
Library:
Instrument: Illumina HiSeq 4000
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: PAIRED
Construction protocol: 5 million cells per condition were collected by 300xg centrifugation and resuspended in 900µl 1X PBS at room temperature. Cells were fixed by the addition of 60µl of 16% fresh formaldehyde (1% final conc., Pierce) followed by an incubation of 10 minutes at room temperature, with rotation. The reaction was stopped by adding glycine 1M to a final concentration of 0.14M, followed by another incubation of 10 minutes at room temperature, with rotation. Cells were collected by centrifugation at 3000 rpm for 5 minutes at 4°C and washed once with 1X PBS. Aliquots of 1 million cells were flash frozen and stored at -80°C. To lyse the cells for ChIP, cells were thawed and resuspended with 1mL of lysis buffer 1 (10mM Tris-HCl pH 8.0, 0.25% Triton X-100, 10mM EDTA, 0.5mM EGTA, 1x Protease inhibitors, and 1mM PMSF), then incubated with rotation for 15 minutes at room temperature. Nuclei were pelleted by centrifugation at 1465 g for 5 minutes at 4°C. Nuclei were then resuspended with 1mL of lysis buffer 2 (10mM Tris-HCl pH 8.0, 200mM NaCl, 10mM EDTA, 0.5mM EGTA, 1x Protease inhibitors, and 1mM PMSF), then incubated with rotation for 10 minutes at 4°C. Nuclei were pelleted by centrifugation at 1465 g for 5 minutes at 4°C. Nuclei were then resuspended in 900uL of lysis buffer 3 (10mM Tris-HCl pH 8.0, 10mM EDTA, 0.5mM EGTA, 0.1% SDS, 1x Protease inhibitors, and 1mM PMSF) and sonicated in a Covaris M220 instrument (PIP = 75; CPB = 200; Duty Factor = 20%; Time = 10 minutes; Setpoint temperature = 7°C) using a 1mL AFA Fiber milliTube (Covaris). The sonicated lysate was centrifuged at max. speed for 10 minutes at 4°C, and the supernatant was retained. 30uL of Protein A Dynabeads (Invitrogen 10001D) were washed three times with ChIP dilution buffer (16.7mM Tris-HCl pH 8.0, 0.01% SDS, 1.1% Triton X-100, 1.2mM EDTA, and 167mM NaCl), each wash consisting of addition of 1mL of buffer and collection of the beads on a magnetic rack. The 30uL beads were then resuspended in 900uL of dilution buffer and combined with the ChIP sample to pre-clear the sample. Beads and chromatin were incubated with rotation for 2 hours at 4°C. Beads were then collected on a magnetic rack and the supernatant was retained. 2uL of SNAP-ChIP K-MetStat panel (EpiCypher, 19-1001) was added to the sample chromatin. SNAP-ChIP K-MetStats are barcoded recombinant nucleosomes bearing distinct methyl-lysine modifications and was used as spike-in controls for ChIP reactions. 1% of the sample was saved as Input, the rest was used for ChIP. 2uL of antibody (Cell Signaling; anti-H3K27me3 (9733S), (Cell Singaling; anti-H3K36me2 (2901S)) was added to the ChIP sample. The samples were then rotated overnight at 4°C. 60uL of Protein A Dynabeads were washed three times with 1mL of ChIP dilution buffer and resuspended in 60uLof dilution buffer. Beads were then added to the ChIP sample and rotated for 2 hours at 4°C. The beads were then washed twice with Wash buffer A (50mM HEPES pH 7.9, 1% Triton X-100, 0.1% Deoxycholate, 1mM EDTA, and 140mM NaCl), with Wash buffer B (50mM HEPES pH 7.9, 0.1% SDS, 1% Triton X-100, 0.1% Deoxycholate, 1mM EDTA, and 500mM NaCl), and with TE buffer (10mM TrisHCl pH 8.0, 1mM EDTA). Each wash consists of resuspension in 500μL buffer and rotation for 4 minutes, followed by collection of beads and removal of supernatant. DNA was eluted in 100μL elution buffer (50mM TrisHCl pH 8.0, 1mM EDTA, and 1% SDS) at 65°C for 10 minutes shaking at 1400RPM on orbital shaker. The eluent was collected and the beads were subjected to a second round of elution with 150μL elution buffer. The ChIP eluants were pooled, and the input sample was diluted to 250μL with elution buffer. These samples were incubated at 65°C overnight to promote decrosslinking. The samples were then allowed to cool to room temperature, 15μg of RNAse A (PureLink, Invitrogen) was added, and the samples were incubated at 37°C for 30 minutes to degrade RNA. 100μg Proteinase K was then added and the samples were incubated at 56°C for two hours. DNA was purified using a MinElute PCR Purification kit (Qiagen). DNA was sonicated again to 150bp average fragment size with a Covaris M220 instrument (PIP = 75; CPB = 200; Duty Factor = 20%; Time = 10 minutes; Setpoint temperature = 20°C) and libraries were generated using the Accel-NGS 2S Plus DNA Library Kit (Swift). Accel-NGS 2S Plus DNA Library Kit
Experiment attributes:
GEO Accession: GSM5653825
Links:
Runs: 1 run, 29M spots, 8.7G bases, 3.4Gb
Run# of Spots# of BasesSizePublished
SRR1656227529,038,9408.7G3.4Gb2022-03-30

ID:
17365330

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