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Blood, 15 May 2001, Vol. 97, No. 10, pp. 3032-3039
HEMATOPOIESIS
Inhibitory effect of the mi transcription factor
encoded by the mutant mi allele on GA binding
protein-mediated transcript expression in mouse mast
cells
Eiichi Morii,
Hideki Ogihara,
Keisuke Oboki,
Chika Sawa,
Takahiko Sakuma,
Shintaro Nomura,
Jeffrey D. Esko,
Hiroshi Handa, and
Yukihiko Kitamura
From the Department of Pathology, Osaka University
Medical School, Suita, Japan; the Research Function of Biotechnology,
Frontier Collaborative Research Center, Tokyo Institute of Technology,
Yokohama, Japan; and the Division of Cellular and Molecular Medicine,
Glycobiology Program, University of California, San Diego, CA.
The mi transcription factor (MITF) is a
basic-helix-loop-helix leucine zipper (bHLH-Zip) transcription factor
that is important for the development of mast cells. Mast cells of
mi/mi genotype express normal amounts of abnormal MITF
(mi-MITF), whereas mast cells of tg/tg genotype
do not express any MITFs. The synthesis of heparin is abnormal in the
skin mast cells of mi/mi mice. Because N-deacetylase/N-sulfotransferase 2 (NDST-2) is essential for the synthesis of heparin, the amount of NDST-2 messenger RNA (mRNA) was compared among cultured mast cells (CMCs) of +/+,
mi/mi, and tg/tg genotypes. The NDST-2 mRNA was
detected by in situ hybridization in the skin mast cells of +/+ and
tg/tg mice, but not in the skin mast cells of
mi/mi mice. The amount of NDST-2 mRNA decreased significantly in CMCs derived from mi/mi mice when compared
to the values of +/+ and tg/tg mice, suggesting that the
defective form of MITF inhibited the expression of the NDST-2
transcript. The expression of NDST-2 transcript was mediated by the
GGAA motif located in the 5'-untranslated region. GA binding protein
(GABP) bound the GGAA motif and increased the amount of NDST-2
transcript. The mi-MITF appeared to inhibit the ability of
GABP to express NDST-2 transcript by disturbing its nuclear
localization. This is the first study to show that expression of an
abnormal form of a bHLH-Zip transcription factor can dramatically alter
the intracellular location of another DNA/RNA binding factor, which in
turn brings about profound and unexpected consequences on transcript expression.
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