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Blood, Vol. 92 No. 6 (September 15), 1998:
pp. 1973-1980
Impaired Expression of Integrin  -4 Subunit in Cultured Mast Cells
Derived From Mutant Mice of mi/mi Genotype
Dae-Ki Kim,
Eiichi Morii,
Hideki Ogihara,
Koji Hashimoto,
Kenji Oritani,
Young-Mi Lee,
Tomoko Jippo,
Shiro Adachi,
Yuzuru Kanakura, and
Yukihiko Kitamura
From the Department of Pathology, the Department of Internal Medicine
II, the Department of Hematology and Oncology, Osaka University Medical
School, Suita, Japan.
The mi locus encodes a member of the
basic-helix-loop-helix-leucine zipper protein family of transcription
factors (hereafter called MITF). We have reported that expression of
several genes was impaired in cultured mast cells (CMCs) of
mi/mi mice due to a defective transactivation ability of mutant
MITF (mi-MITF). Because attachment of mi/mi CMCs to
fibroblasts is impaired, we examined the expression of integrin genes
in mi/mi CMCs in the present study. Among the integrin genes
examined, the expression of integrin  4 subunit was barely detectable
in mi/mi CMCs, and the 4 protein was not detected by flow
cytometry either. The specific adhesion to vascular cell adhesion
molecule-1 (VCAM-1), the ligand for 4 subunit, was
observed in +/+ CMCs but not in mi/mi CMCs, indicating that
the expression of integrin 4 subunit at a functional level did not
occur in mi/mi CMCs. In the promoter region of the 4 subunit
gene, there was a CACTTG motif to which normal MITF (+- MITF) bound.
The coexpression of +-MITF but not of mi-MITF transactivated
the promoter of the 4 subunit gene. The deletion or mutation of the
CACTTG motif abolished the transactivation by +-MITF, suggesting that
+-MITF directly transactivated the gene encoding 4 subunit of
integrin.
© 1998 by The American Society of Hematology.
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