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| Status |
Public on Oct 04, 2013 |
| Title |
TRIM28 is essential for erythroblast differentiation in the mouse |
| Organism |
Mus musculus |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
We discovered that Trim28 genetic loss in the adult mouse leads to defective immature erythropoiesis in the bone marrow and consequently to anemia.We further found that TRIM28 controls erythropoiesis in a cell-autonomous manner by inducibly deleting Trim28 exclusively in hematopoietic cells. Finally, in the absence of TRIM28 we observed increased apoptosis as well as diminished expression of multiple erythroid transcription factors and heme biosynthetic enzymes in immature erythroid cells. Thus, TRIM28 is essential for the cell-autonomous development of immature erythroblasts in the bone marrow.
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| Overall design |
To induce Cre recombinase from the Mx1Cre transgene, poly(I:C) was injected 5 times every other day. Mice were analyzed two weeks after completion of poly(I:C) administration. TRIM28 mutant mice generate two distinct types of immature erythroid cells; KOa, with 5-8% of the Trim28 gene remaining undeleted (still bearing 26% of residual mRNA), and KOb, with 1-4% of the gene remaining undeleted (and with 18% of mRNA remaining).
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| Contributor(s) |
Hosoya T, Engel JD |
| Citation(s) |
24092935 |
| |
| Submission date |
Aug 13, 2013 |
| Last update date |
May 15, 2019 |
| Contact name |
Tomonori Hosoya |
| Organization name |
University of Michigan
|
| Department |
CDB
|
| Lab |
Engel
|
| Street address |
109 Zina Pitcher Place
|
| City |
Ann Arbor |
| State/province |
MI |
| ZIP/Postal code |
48109 |
| Country |
USA |
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| Platforms (1) |
| GPL13112 |
Illumina HiSeq 2000 (Mus musculus) |
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| Samples (9)
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| Relations |
| BioProject |
PRJNA215083 |
| SRA |
SRP028806 |
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