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Blood, 15 February 2008, Vol. 111, No. 4, pp. 1924-1932.
Prepublished online as a Blood First Edition Paper on December 6, 2007; DOI 10.1182/blood-2007-08-104489.
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Submitted August 3, 2007
Accepted November 19, 2007
Differential context-dependent effects of FOG-1 on mast cell development and differentiation
Daijiro Sugiyama, Makoto Tanaka, Kenji Kitajima, Jie Zheng, Hilo Yen, Tomotaka Murotani, Atsushi Yamatodani, and Toru Nakano*
Department of Stem Cell Pathology, Medical School and Graduate School of Fronteir Biosciences, Osaka University, Suita, Osaka, Japan
Department of Medical Physics and Engineering, Division of Health Sciences, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan
* Corresponding author; email: tnakano{at}patho.med.osaka-u.ac.jp.
Friend of GATA-1 (FOG-1) is a binding partner of GATA-1, a zinc finger transcription factor with crucial roles in erythroid, megakaryocytic, and mast cell differentiation. FOG-1 is indispensable for the function of GATA-1 during erythro/megakaryopoiesis, but FOG-1 is not expressed in mast cells. Here, we analyzed the role of FOG-1 in mast cell differentiation using a combined experimental system with conditional gene expression and in vitro hematopoietic induction of mouse embryonic stem cells. Expression of FOG-1 during the progenitor period inhibited the differentiation of mast cells and enhanced the differentiation of neutrophils. Analysis using a mutant of PU.1, a transcription factor that positively or negatively cooperates with GATA-1, revealed that this lineage skewing was caused by disrupted binding between GATA-1 and PU.1, which is a prerequisite for mast cell differentiation. However, FOG-1 expression in mature mast cells brought about a reversible loss of the mast cell phenotype. In contrast to the lineage skewing, the loss of the mast cell phenotype was caused by down-regulation of MITF, a bHLH transcription factor required for mast cell differentiation and maturation. These results indicate that FOG-1 inhibits mast cell differentiation in a differentiation stage-dependent manner and its effects are produced via different molecular mechanisms.
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