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Blood, 1 February 2001, Vol. 97, No. 3, pp. 645-651
HEMATOPOIESIS
Inhibitory effect of the transcription factor encoded by the
mutant mi microphthalmia allele on transactivation of mouse
mast cell protease 7 gene
Hideki Ogihara,
Eiichi Morii,
Dae-Ki Kim,
Keisuke Oboki, and
Yukihiko Kitamura
From the Department of Pathology, Osaka University
Medical School, Suita, Japan.
The transcription factor encoded by the mi locus
(MITF) is a transcription factor of the basic-helix-loop-helix zipper
protein family. Mice of mi/mi genotype express a
normal amount of abnormal MITF, whereas mice of
tg/tg genotype do not express any MITFs due
to the transgene insertional mutation. The effect of normal (+) and
mutant (mi) MITFs on the expression of mouse mast cell protease (MMCP) 6 and 7 was examined. Both MMCP-6 and MMCP-7 are tryptases, and their coding regions with high homology are closely located on chromosome 17. Both MMCP-6 and MMCP-7 genes are expressed in
normal cultured mast cells (+/+ CMCs). Although the
transcription of MMCP-6 gene was severely suppressed in both
mi/mi and tg/tg CMCs, that
of MMCP-7 gene was severely suppressed only in mi/mi CMCs.
The study identified the most significant segment for the transcription
in the 5' flanking region of MMCP-7 gene. Unexpectedly, no CANNTG
motifs were found that are recognized and bound by +-MITF in this
segment. Instead, there was an AP-1 binding motif, and binding of c-Jun
to the AP-1 motif significantly enhanced the transcription of MMCP-7
gene. The complex formation of c-Jun with either +-MITF or
mi-MITF was demonstrated. The binding of +-MITF to c-Jun
enhanced the transactivation of MMCP-7 gene, and that of
mi-MITF suppressed the transactivation. Although the former complex was located only in the nucleus, the latter complex was predominantly found in the cytoplasm. The negative effect of
mi-MITF on the transcription of MMCP-7 gene appeared to be
executed through the interaction with c-Jun.
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