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Blood, Vol. 93 No. 6 (March 15), 1999:
pp. 1942-1950
Deficient Transcription of Mouse Mast Cell Protease 4 Gene in
Mutant Mice of mi/mi Genotype
Tomoko Jippo,
Young-Mi Lee,
Yee Katsu,
Kumiko Tsujino,
Eiichi Morii,
Dae-Ki Kim,
Hyung-Min Kim, and
Yukihiko Kitamura
From the Department of Pathology, Osaka University Medical School,
Suita, Japan; and the Department of Oriental Pharmacy, College of
Pharmacy, Wonkwang University, Chonbuk, Korea.
The mi locus encodes a member of the
basic-helix-loop-helix-leucine zipper (bHLH-Zip) protein family of
transcription factors (hereafter called MITF). We reported that
expression of the mouse mast cell protease 5 (MMCP-5) and MMCP-6 genes
were deficient in cultured mast cells (CMC) derived from mutant mice of
mi/mi genotype. Despite the reduced expression of both MMCP-5
and MMCP-6, their regulation mechanisms were different. Because MMCP-5
is a chymase and MMCP-6 a tryptase, there was a possibility that the
difference in regulation mechanisms was associated with their different
characteristics as proteases. We compared the regulation mechanisms of
another chymase, MMCP-4, with those of MMCP-5 and MMCP-6. The
expression of the MMCP-4 gene was also deficient in mi/mi CMC.
The overexpression of the normal (+) MITF but not of mi-MITF
normalized the poor expression of the MMCP-4 gene in mi/mi CMC,
indicating the involvement of +-MITF in transactivation of the MMCP-4
gene. Although MMCP-4 is chymase as MMCP-5, the regulation of MMCP-4
expression was more similar to MMCP-6 than to MMCP-5. We also showed
the deficient expression of granzyme B and cathepsin G genes in
mi/mi CMC. Genes encoding granzyme B, cathepsin G, MMCP-4, and
MMCP-5 are located on chromosome 14. Because all these genes showed
deficient expression in mi/mi CMC, there is a possibility that
MITF might regulate the expression of these genes through a locus
control region.
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