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SRX19051702: GSM6938945: ChIPseq-H3K4me1; Homo sapiens; ChIP-Seq
1 ILLUMINA (NextSeq 500) run: 17.1M spots, 1.2G bases, 512.1Mb downloads

External Id: GSM6938945_r1
Submitted by: Martin Eilers, Chair for Biochemistry and Molecular Biology, University of Wuerzburg
Study: TFIIIC and MYCN link the three-dimensional chromatin structure of promoters to transcription termination of stalled RNA polymerase (ChIPseq CnR)
show Abstracthide Abstract
MYC proteins bind to virtually all active promoters transcribed by RNA polymerase II (RNAPII), but whether they interact with the three-dimensional chromatin architecture is unknown. Here we used HiChIP sequencing of the MYCN oncoprotein and found that MYCN localizes to three-dimensional hubs formed by active promoters and enhancers. In these hubs, MYCN interacts with TFIIIC, an architectural protein complex. MYCN recruits TFIIIC to promoters when transcription elongation is inhibited, and the complex of both proteins induces premature transcription termination. Termination correlates closely with the TFIIIC-dependent removal of MYCN from promoter hubs and with corresponding alterations in the three-dimensional interactions of cohesin complexes. This limits DNA damage by removing RNAPII that stalls proximal to double-strand breaks. Binding of TFIIIC to MYCN is limited by competition with Aurora-A and this protects genes involved in mRNA processing from termination, arguing that MYCN contributes to the unusual proliferative capacity of neuroblastoma cells via removing stalled RNAPII from promoter hubs and via increasing the capacity for RNA processing. Overall design: CUT&RUN, ChIP and ChIP-Rx DNA-sequencing was done with SH-EP NMYC-ER cells where the NMYC expression can be induced with 4-OHT. For all CUT&Run sequencing and some ChIP-seq and ChIP-Rx sequencing experiments, SH-EP NMYC-ER cells were used that carry a doxycycline inducible shRNA against TF3C5. For CUT&Run sequencing samples, the immunoprecipitation of digested DNA was done for EXOSC5 with or without NMYC expression and with or without expression of shTF3C5. As control, DNA was sequenced following immunoprecipitation with an unspecific IgG antibody. For ChIP-seq and ChIP-Rx sequencing experiments, the immunopresipitated antibodies are listed below. All experiments were done with or without NMYC expression and where indicated, a shRNA targeting TF3C5 was induced via doxycycline or one of the below listed inhibitors was applied.
Sample: ChIPseq-H3K4me1
SAMN32769681 • SRS16468173 • All experiments • All runs
Organism: Homo sapiens
Library:
Name: GSM6938945
Instrument: NextSeq 500
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: For Cut&Run sequencing, cells were harvested with Accutase, washed and then coupled to ConA-coated magentic beads (Polysciences Europe). Cells were then permeabilized and incubated with the primary antibody (EXOSC5 #NBP2-14952; 1:100 diluted; Novus Biologicals) in antibody binding buffer over night at 4°C. Cells were then washed in the presence of digitonin and 700 ng/ml MNase was added per sample for 1 hour at 4°C. For Cut&Run sequencing samples, the MNase treated cells were washed with low-salt rinse buffer. Incubation buffer, containing CaCl2 and digitonin, was added for 30 min at 4°C. The Mnase activity was stoped in the presence of 20 µg/ml Rnase A. DNA fragments were released at 37°C for 30 min and the decrosslinking was done for 1 hour at 50°C by adding 0.01% SDS and 10 mg/ml Proteinase K. DNA was extracted wit phenol-chloroform and resuspended in TE buffer. For ChIP-seq and ChIP-Rx sequencing, cells were fixed for 5 min at RT with 1% formaldehyde and harvested in cold PBS contianing protease and phosphatase inhibitors. For ChIP-Rx samples, murine NHO2A or NIH3T3 cells were added at a 1:10 cell ratio during cell lysis to serve as an exogenous control (spike-in). Cell lysis was done for 20 min in PIPES buffer containing 85 mM KCl and 0.5% NP-40, followed by collection of nuclei by centrifugation. For ChIP-seq and ChIP-Rx sequencing, the crosslinked chromatin was extracted from the nuclei in TRIS buffer with 150 mMCaCl, 1 mM EDTA and 1% NP-40, 1% sodium deoxycholate and 0.1% SDS. The chromatin was fragmented using the Covaris Focused Ultrasonicator M220 for 50 min. Dynabeads Protein A and Protein G were pre-incubated overnight with 10-15 µg antibody in the presence of 5 mg/ml BSA. For ChIP-seq and ChIP-Rx sequencing, chromatin was added to the pre-incubated beads for at least 6h at 4°C with rotation. Beads were then washed with different TRIS buffers containing distinct salt-concentrations, EDTA and detergents, followed by wahsing with only TE-buffer. Chromatin was eluted with 100mM NaHCO3 and 1% SDS for 15 min. Protein and RNA were digested with proteinase K and RNase A. DNA was isolated by phenol-chloroform extraction followed by an ethanol precipitation. DNA was quantified using the Quant-IT PicoGreen dsDNA assay. The DNA libraries were prepared using the NEBNext Ultra II DNA Library Prep Kit for Illumina (New England Biolabs) according to the manufacturer's instructions. Pre-PCR samples were purified and/or size-selected using AMPureXP beads. The libraries were PCR-amplified with the NEBNext Multiplex Oligos for Illumina Kit and again purified using Agencourt AMPure XP beads (Beckman Coulter). Library quality and fragment size distribution was analyzed on a Fragment Analyzer (Advanced Analytical). Sequencing was performed in single-read or paired-end mode on a NextSeq500 or NextSeq2000 platform (Illumina). ChIP, ChIP-Rx and CUT&RUN followed by sequencing.
Runs: 1 run, 17.1M spots, 1.2G bases, 512.1Mb
Run# of Spots# of BasesSizePublished
SRR2309952817,072,1311.2G512.1Mb2023-01-19

ID:
26222389

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