|
| Status |
Public on Oct 30, 2014 |
| Title |
Genome-wide chromatin analysis of Ewing sarcoma (RNA-seq) |
| Organism |
Homo sapiens |
| Experiment type |
Expression 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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| |
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| Overall design |
Ewing sarcoma cell lines (A673 and SKNMC) were analyzed by RNA-seq. EWS-FLI1 was depleted by infection with lentiviral shRNAs (shFLI1 and shGFP control).
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| |
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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) |
[email protected]
|
| 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) |
| GPL11154 |
Illumina HiSeq 2000 (Homo sapiens) |
|
| Samples (6)
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| This SubSeries is part of SuperSeries: |
| GSE61953 |
Genome-wide chromatin analysis of Ewing sarcoma |
|
| Relations |
| BioProject |
PRJNA262778 |
| SRA |
SRP048562 |
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