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J. Biol. Chem., Vol. 278, Issue 1, 233-240, January 3, 2003
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From the Department of Pathology, Nagoya University School of
Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Aichi,
Japan
Microtubule-associated protein MAP1A is expressed
abundantly in mature neurons and is necessary for maintenance of
neuronal morphology and localization of some molecules in association
with the microtubule-based cytoskeleton. Previous studies indicated that its complementary expression together with MAP1B during nervous system development is regulated at the transcriptional level and that
the mouse Map1A gene is transcribed under the
control of 5' and intronic promoters. In this study, we investigated
the regulatory mechanisms that govern the neuronal cell-specific
activation of the MAP1A 5' promoter. We found that two
regulatory factor for X box (RFX) binding sites in exon1 of both the
mouse and human genes are important for effective transcriptional
repression observed only in non-neuronal cells by reporter assays.
Among RFX transcription factor family members, RFX1 and 3 mainly
interact with repressive elements in vitro. Cotransfection
studies indicated that RFX1, which is expressed ubiquitously,
down-regulated the MAP1A 5' promoter activity in
non-neuronal cells. Unexpectedly, RFX3, which is abundantly expressed
in neuronal cells, down-regulated the transactivity as well, when it
was expressed in non-neuronal cells. Both RFX1 and 3 did not
down-regulate the transactivity in neuronal cells. These results
suggest that RFX1 and 3 are pivotal factors in down-regulation of the
MAP1A 5' promoter in non-neuronal cells. The cell
type-specific down-regulation, however, does not depend simply on which
RFX interacts with the elements, but seems to depend on underlying profound mechanisms.
Role for RFX Transcription Factors in Non-neuronal
Cell-specific Inactivation of the Microtubule-associated Protein
MAP1A Promoter*
,
*
This work was supported in part by a grant for COE research
from the Ministry of Education, Science, Culture and Sports in Japan.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Department of
Embryology, Institute for Developmental Research, Aichi Human Service Center, Kamiya-cho, Kasugai, Aichi 480-0392, Japan. Tel.:
81-568-88-0811; Fax: 81-568-88-0829; E-mail:
k46191a@nucc.cc.nagoya-u.ac.jp.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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