|
| Status |
Public on Oct 30, 2014 |
| Title |
Genome-wide chromatin analysis of Ewing sarcoma (ATAC-seq) |
| Organism |
Homo sapiens |
| Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
|
| Summary |
We show that EWS-FLI1, an aberrant transcription factor responsible for the pathogenesis of Ewing sarcoma, reprograms gene regulatory circuits by directly inducing or directly repressing enhancers. At GGAA repeats, which lack regulatory potential in other cell types and are not evolutionarily conserved, EWS- FLI1 multimers potently induce chromatin opening, recruit p300 and WDR5, and create de novo enhancers. GGAA repeat enhancers can loop to physically interact with target promoters, as demonstrated by chromosome conformation capture assays. Conversely, EWS-FLI1 inactivates conserved enhancers containing canonical ETS motifs by displacing wild-type ETS transcription factors and abrogating p300 recruitment.
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| Overall design |
Mesenchymal stem cells (MSCs) and a Ewing sarcoma cell line (SKNMC) were analyzed by ATAC-seq. EWS-FLI1 was expressed in MSCs using a lentiviral vector (pLIV EWSFLI1 or pLIV empty vector control).
* Raw data not provided for the MSC samples. *
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| Contributor(s) |
Aryee M, Rivera M |
| Citation(s) |
25453903 |
| Submission date |
Oct 01, 2014 |
| Last update date |
May 15, 2019 |
| Contact name |
Martin Aryee |
| E-mail(s) |
aryee.martin@mgh.harvard.edu
|
| Organization name |
Massachusetts General Hospital
|
| Department |
Pathology
|
| Street address |
149 13th Street
|
| City |
Charlestown |
| State/province |
MA |
| ZIP/Postal code |
02129 |
| Country |
USA |
| |
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| Platforms (1) |
| GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
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| Samples (3) |
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| This SubSeries is part of SuperSeries: |
| GSE61953 |
Genome-wide chromatin analysis of Ewing sarcoma |
|
| Relations |
| BioProject |
PRJNA262779 |
| SRA |
SRP048563 |
