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Blood, 1 March 2006, Vol. 107, No. 5, pp. 1857-1863.
Prepublished online as a Blood First Edition Paper on October 27, 2005; DOI 10.1182/blood-2005-06-2527.
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HEMATOPOIESIS
Redirecting differentiation of hematopoietic progenitors by a transcription factor, GATA-2
Kenji Kitajima,
Makoto Tanaka,
Jie Zheng,
Hilo Yen,
Ayuko Sato,
Daijiro Sugiyama,
Hiroki Umehara,
Eiko Sakai, and
Toru Nakano
From the Department of Pathology, Medical School and Graduate School of Frontier Biosciences, Department of Molecular Cell Biology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
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.
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