|
| Status |
Public on Jan 12, 2016 |
| Title |
The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Dot1l ko RNA-seq] |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML
Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector.
Results: Inactivation of either Dot1l or Mll1 in this model leads to a substantial delay or complete abrogation of leukemia development. Loss of Dot1l or Mll1 are associated with gene expression changes that have substantial overlap. In addition, genes that are downregulated follwing inactivation of Dot1l or Mll1 have substantial overlap with the gene set upregulated in MN1 transduced CMPs.
Conclusions: MN1 mediated leukemogenesis is associated with a gene expression program that dependes on Mll1 and Dot1l
|
| |
|
| Overall design |
Examination of mRNA levels between Dot1l f/f and Dot1l ko, and Mll1 f/f and Mll1 ko.
|
| |
|
| Contributor(s) |
Riedel S, Bernt K |
| Citation(s) |
26927674 |
| |
| Submission date |
Jan 11, 2016 |
| Last update date |
May 15, 2019 |
| Contact name |
Tobias Neff |
| E-mail(s) |
[email protected]
|
| Phone |
303-724-7445
|
| Organization name |
University of Colorado Denver AMC
|
| Department |
Pediatric Oncology
|
| Lab |
Neff
|
| Street address |
12800 E. 19th Ave.
|
| City |
Aurora |
| State/province |
CO |
| ZIP/Postal code |
80045 |
| Country |
USA |
| |
|
| Platforms (1) |
| GPL13112 |
Illumina HiSeq 2000 (Mus musculus) |
|
| Samples (6)
|
|
| This SubSeries is part of SuperSeries: |
| GSE76750 |
The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML |
|
| Relations |
| BioProject |
PRJNA308488 |
| SRA |
SRP068319 |
Less...
More...