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 Blood, 1 February 2008, Vol. 111, No. 3, pp. 1138-1146.
Prepublished online as a Blood First Edition Paper on October 12, 2007; DOI 10.1182/blood-2007-07-098202.

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HEMATOPOIESIS

The role of Ikaros in human erythroid differentiation

Marilyne Dijon13, Florence Bardin13, Anne Murati2,4, Michèle Batoz5, Christian Chabannon13, and Cécile Tonnelle14

1 Centre de Thérapie Cellulaire et Génique, Institut Paoli-Calmettes, Marseille; 2 Inserm U599, Centre de Recherche en Cancérologie de Marseille, Marseille; 3 Université de la Méditerranée, Marseille; 4 Département de Biopathologie, Institut Paoli-Calmettes, Marseille; and 5 Inserm U576, Hôpital l'Archet, Nice, France

Ikaros—a factor that positively or negatively controls gene transcription—is active in murine adult erythroid cells, and involved in fetal to adult globin switching. Mice with Ikaros mutations have defects in erythropoiesis and anemia. In this paper, we have studied the role of Ikaros in human erythroid development for the first time. Using a gene-transfer strategy, we expressed Ikaros 6 (Ik6)—a known dominant-negative protein that interferes with normal Ikaros activity—in cord blood or apheresis CD34+ cells that were induced to differentiate along the erythroid pathway. Lentivirally induced Ik6-forced expression resulted in increased cell death, decreased cell proliferation, and decreased expression of erythroid-specific genes, including GATA1 and fetal and adult globins. In contrast, we observed the maintenance of a residual myeloid population that can be detected in this culture system, with a relative increase of myeloid gene expression, including PU1. In secondary cultures, expression of Ik6 favored reversion of sorted and phenotypically defined erythroid cells into myeloid cells, and prevented reversion of myeloid cells into erythroid cells. We conclude that Ikaros is involved in human adult or fetal erythroid differentiation as well as in the commitment between erythroid and myeloid cells.


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