U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination

SRX4579166: GSM3347549: H3K36me2_ChIPseq_mESCs; Drosophila melanogaster; Mus musculus; ChIP-Seq
1 ILLUMINA (Illumina HiSeq 4000) run: 65M spots, 3.2G bases, 1.5Gb downloads

Submitted by: NCBI (GEO)
Study: H3K36me2 recruits DNMT3A and shapes intergenic DNA methylation landscapes
show Abstracthide Abstract
Enzymes catalyzing CpG methylation in DNA, including DNMT1 and DNMT3A/B, are indispensable for mammalian tissue development and homeostasis. They are also implicated in human developmental disorders and cancers, supporting a critical role of DNA methylation during cell fate specification and maintenance. Recent studies suggest that histone post-translational modifications (PTMs) are involved in specifying patterns of DNMT localization and DNA methylation at promoters and actively transcribed gene bodies. However, mechanisms governing the establishment and maintenance of intergenic DNA methylation remain poorly understood. Germline mutations in DNMT3A lead to a childhood overgrowth syndrome that is phenotypically overlapping with Sotos syndrome caused by haploinsufficiency of NSD1, a histone methyltransferase catalyzing di-methylation on H3K36 (H3K36me2), pointing to a potential mechanistic link between the two disorders. Here we report that NSD1-mediated H3K36me2 is required for recruitment of DNMT3A and maintenance of DNA methylation at intergenic regions. Genome-wide analysis shows binding and activity of DNMT3A are co-localized with H3K36me2 at non-coding regions of euchromatin. Genetic ablation of NSD1 and its paralogue NSD2 in mouse and human cells redistributes DNMT3A to H3K36me3-marked gene bodies and reduces intergenic DNA methylation. NSD1 mutant tumors and Sotos patient samples are also associated with intergenic DNA hypomethylation. Consistently, PWWP-domain of DNMT3A shows dual recognition of H3K36me2/3 in vitro with a higher binding affinity towards H3K36me2, which is abrogated by overgrowth syndrome-derived missense mutations. Taken together, our study uncovers a trans-chromatin regulatory pathway that, when perturbed, promotes neoplastic and developmental overgrowth. Overall design: WGBS, RNA-seq, and ChIP-seq for DNMT proteins and histone H3 post-translational modifications in C3H10T1/2 cells. WGBS and ChIP-seq for H3K36me2 in human head and neck squamous cell carcinoma cell lines and mouse embryonic stem cells.
Sample: H3K36me2_ChIPseq_mESCs
SAMN09864099 • SRS3693599 • All experiments • All runs
Library:
Instrument: Illumina HiSeq 4000
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: To obtain a soluble chromatin extract, ~2x10^7 cells were resuspended in 1 mL LB1 (50 mM HEPES, 140 mM NaCl, 1 mM EDTA, 10% glycerol, 0.5% NP-40, 0.25% Triton X-100, 1x Complete protease inhibitor) and incubated rotating at 4°C for 10 min. Samples were centrifuged, resuspended in 1 mL LB2 (10 mM Tris-HCl pH 8.0, 200 mM NaCl, 1 mM EDTA, 0.5 mM EGTA, 1x Compete protease inhibitor), and incubated rotating at 4°C for 10 min. Finally, samples were centrifuged, resuspended in 1 mL LB3 (10 mM Tris-HCl pH 8.0, 100 mM NaCl, 1 mM EDTA, 0.5 mM EGTA, 0.1% Na deoxycholate, 0.5% N-lauroylsarcosine, 1% Triton X-100, 1x Complete protease inhibitor), and homogenized by passing two times through a 27-gauge needle. Chromatin extracts were sonicated for 8 min (anti-HA ChIP) or 12 min (anti-histone PTM ChIP) using a Covaris E220 focused ultra-sonicator at peak power 140, duty factor 5, and cycles/burst 200. For histone PTM ChIP-Rx, after centrifugation soluble chromatin was spiked-in with soluble chromatin from Drosophila S2 cells that was similarly prepared and equivalent to 5-10% of the mouse/human cell chromatin. The lysates were incubated with 100 μl Pierce anti-HA beads (Themo Scientific, 88836) or with anti-H3K4me1 (Abcam, ab8895), anti-H3K9me3 (Abcam, ab8898), anti-H3K27ac (Active Motif, 39133), anti-H3K27me3 (Cell Signaling Tech, 9733), anti-H3K36me2 (Cell Signaling, 2901) or anti-H3K36me3 (Active Motif, 61101) antibody bound to 75 μl protein A or protein G Dnya1 magnetic beads (Invitrogen) and incubated overnight at 4°C with 5% kept as input DNA. Magnetic beads were washed with low salt buffer (150 mM NaCl; 0.1% SDS; 1% Triton X-100; 1 mM EDTA; 50 mM Tris-HCl), high salt buffer (500 mM NaCl; 0.1% SDS; 1% Triton X-100; 1 mM EDTA; 50 mM Tris-HCl), LiCl buffer (150 mM LiCl; 0.5% Na deoxycholate; 0.1% SDS; 1% Nonidet P-40; 1 mM EDTA; 50 mM Tris-HCl) and TE buffer (1 mM EDTA; 10 mM Tris-HCl). For ChIP-seq, beads were resuspended in elution buffer (1% SDS, 50 mM Tris-HCl pH 8.0, 10mM EDTA, 200 mM NaCl) and incubated for 30 min at 65°C. After centrifugation the eluate was reverse cross-linked overnight at 65°C. The eluate was then treated with RNaseA for 1 hr at 37°C and with Proteinase K (Roche) for 1 hr at 55°C and DNA was recovered using Qiagen PCR purification kit. KAPA HTP Library Preparation Kit
Experiment attributes:
GEO Accession: GSM3347549
Links:
Runs: 1 run, 65M spots, 3.2G bases, 1.5Gb
Run# of Spots# of BasesSizePublished
SRR772230964,997,0123.2G1.5Gb2019-08-30

ID:
6191075

Supplemental Content

Search details

See more...

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...