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Blood, 15 February 2005, Vol. 105, No. 4, pp. 1448-1455.
Prepublished online as a Blood First Edition Paper on October 26, 2004; DOI 10.1182/blood-2003-11-4068.
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HEMATOPOIESIS
Gfi-1B plays a critical role in terminal differentiation of normal and transformed erythroid progenitor cells
Loïc Garçon,
Catherine Lacout,
Fédor Svinartchouk,
Jean-Pierre Le Couédic,
Jean-Luc Villeval,
William Vainchenker, and
Dominique Duménil
From the Institut National de la Santé et de la Recherche Médicale (INSERM) U362, Institut Gustave Roussy, 39 rue Camille Desmoulins, 94805 Villejuif cedex, France.
Growth factor independence-1B (Gfi-1B) is a transcription factor with a highly conserved transcriptional repressor snail–Gfi-1 (SNAG) domain and 6 zinc-finger domains at the N- and C-terminus, respectively. Disruption of the Gfi-1B gene is lethal in the embryo with failure to produce definitive enucleated erythrocytes. In this study, we analyzed the role of Gfi-1B in human erythropoiesis. We observed an increase of Gfi-1B expression during erythroid maturation of human primary progenitor cells. We studied the consequences of variations in Gfi-1B expression in 2 transformed cell lines (K562 and UT7 cells), as well as in primary CD36+/GPA– progenitors. A knock-down of Gfi-1B delayed the terminal differentiation of K562 and primary cells. Forced expression of Gfi-1B in UT7 and K562 cells led to an arrest of proliferation and an induction of erythroid differentiation. Enforced expression of Gfi-1B in primary cells at the colony-forming units-erythroid (CFU-E) stage led to a partial glycophorin A (GPA) induction after erythropoietin (EPO) withdrawal but failed to protect cells from apoptosis. Deletion of the SNAG repressor domain abolished Gfi-1B–induced erythroid maturation, strongly suggesting that Gfi-1B acts in the late stage of erythroid differentiation as a transcriptional repressor.
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