| First Author | Kitajima K | Year | 2006 |
| Journal | Blood | Volume | 107 |
| Issue | 5 | Pages | 1857-63 |
| PubMed ID | 16254139 | Mgi Jnum | J:129434 |
| Mgi Id | MGI:3769271 | Doi | 10.1182/blood-2005-06-2527 |
| Citation | Kitajima K, et al. (2006) Redirecting differentiation of hematopoietic progenitors by a transcription factor, GATA-2. Blood 107(5):1857-63 |
| abstractText | GATA-2 is a zinc finger transcription factor essential for differentiation of immature hematopoietic cells. We analyzed the function of GATA-2 by a combined method of tetracycline-dependent conditional gene expression and in vitro hematopoietic differentiation from mouse embryonic stem (ES) cells using OP9 stroma cells (OP9 system). In the presence of macrophage colony-stimulating factor (M-CSF), the OP9 system induced macrophage differentiation. GATA-2 expression in this system inhibited macrophage differentiation and redirected the fate of hematopoietic differentiation to other hematopoietic lineages. GATA-2 expression commencing at day 5 or day 6 induced megakaryocytic or erythroid differentiation, respectively. Expression levels of PU.1, a hematopoietic transcription factor that interferes with GATA-2, appeared to play a critical role in differentiation to megakaryocytic or erythroid lineages. Transcription of PU.1 was affected by histone acetylation induced by binding of GATA-2 to the PU.1 promoter region. This study demonstrates that the function of GATA-2 is modified in a context-dependent manner by expression of PU.1, which in turn is regulated by GATA-2. |
