Antagonism of FOG-1 and GATA factors in fate choice for the mast cell lineage

被引:64
作者
Cantor, Alan B. [1 ,2 ]
Iwasaki, Hirorni [4 ]
Arinobu, Yojiro [3 ]
Moran, Tyler B. [1 ]
Shigematsu, Hirokazu [3 ]
Sullivan, Matthew R. [1 ]
Akashi, Koichi [3 ,4 ]
Orkin, Stuart H. [1 ,2 ,5 ]
机构
[1] Childrens Hosp, Div Pediat Hematol Oncol, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Internal Med, Boston, MA 02115 USA
[4] Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka 8128582, Japan
[5] Howard Hughes Med Inst, Boston, MA 02115 USA
关键词
D O I
10.1084/jem.20070544
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The zinc finger transcription factor GATA-1 requires direct physical interaction with the cofactor friend of GATA-1 (FOG-1) for its essential role in erythroid and megakaryocytic development. We show that in the mast cell lineage, GATA-1 functions completely independent of FOG proteins. Moreover, we demonstrate that FOG-1 antagonizes the fate choice of multipotential progenitor cells for the mast cell lineage, and that its down-regulation is a prerequisite for mast cell development. Remarkably, ectopic expression of FOG-1 in committed mast cell progenitors redirects them into the erythroid, megakaryocytic, and granulocytic lineages. These lineage switches correlate with transcriptional down-regulation of GATA-2, an essential mast cell GATA factor, via switching of GATA-1 for GATA-2 at a key enhancer element upstream of the GATA-2 gene. These findings illustrate combinatorial control of cell fate identity by a transcription factor and its cofactor, and highlight the role of transcriptional networks in lineage determination. They also provide evidence for lineage instability during early stages of hematopoietic lineage commitment.
引用
收藏
页码:611 / 624
页数:14
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