International Immunology Advance Access originally published online on June 20, 2005
International Immunology 2005 17(7):847-856; doi:10.1093/intimm/dxh278
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GATA-1 is required for expression of Fc
RI on mast cells: analysis of mast cells derived from GATA-1 knockdown mouse bone marrow
1 Atopy (Allergy) Research Center, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan
2 Biotechnology Research Center, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan
3 Institute of Basic Medical Sciences and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba 305-8577, Japan
Correspondence to: C. Nishiyama; E-mail: chinishi{at}med.juntendo.ac.jp
The high-affinity receptor for IgE (Fc
RI) that is expressed on the surface of mast cells plays an important role in antigen/IgE-mediated allergic reactions. We have previously found that critical elements in the promoter of the FcRI 
- and ß-chain genes are recognized by the transcription factor GATA-1 in electrophoretic mobility shift assays coupled with a transient expression system for the - and ß-chain promoters. To confirm that GATA-1 is involved in the expression of FcRI definitively, we generated bone marrow-derived mast cells from GATA-1 knockdown (KD) heterozygous mice. FACS analysis showed that the frequency of FcRI-positive cells was significantly decreased in mast cells derived from bone marrow of GATA-1 KD mice. Reverse transcription–PCR analysis showed that the level of transcripts not only for GATA-1 but also for both the - and ß-chains was significantly lower in KD mast cells, whereas that of the FcRI 
-chain was not affected. Degranulation caused by cross-linking of FcRI on mast cells prepared from KD mice was markedly repressed in comparison with that of wild-type mast cells. We concluded that the transcription factor GATA-1 positively regulates FcRI - and ß-chain expression and therefore is involved in mast cell development.
Keywords: GATA-1, knockdown mouse, mast cells, transcription factor
Transmitting editor: S. Koyasu
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