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Originally published In Press as doi:10.1074/jbc.M004430200 on October 26, 2000

J. Biol. Chem., Vol. 276, Issue 3, 2180-2188, January 19, 2001
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Molecular Properties of Zic Proteins as Transcriptional Regulators and Their Relationship to GLI Proteins*

Kiyomi MizugishiDagger §, Jun ArugaDagger , Katsunori NakataDagger , and Katsuhiko MikoshibaDagger ||

From the Dagger  Laboratory for Developmental Neurobiology, RIKEN Brain Science Institute, Saitama 351-0198, Japan, § Department of Pediatrics, University of Tokyo, School of Medicine, Tokyo 113-0033, Japan, and || Department of Molecular Neurobiology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan

Zic family genes encode zinc finger proteins, which play important roles in vertebrate development. The zinc finger domains are highly conserved between Zic proteins and show a notable homology to those of Gli family proteins. In this study, we investigated the functional properties of Zic proteins and their relationship to the GLI proteins. We first established an optimal binding sequence for Zic1, Zic2, and Zic3 proteins by electrophoretic mobility shift assay-based target selection and mutational analysis. The selected sequence was almost identical to the GLI binding sequence. However, the binding affinity was lower than that of GLI. Consistent results were obtained in reporter assays, in which transcriptional activation by Zic proteins was less dependent on the GLI binding sequence than GLI1. Moreover, Zic proteins activated a wide range of promoters irrespective of the presence of a GLI binding sequence. When Zic and GLI proteins were cotransfected into cultured cells, Zic proteins enhanced or suppressed sequence-dependent, GLI-mediated transactivation depending on cell type. Taken together, these results suggest that Zic proteins may act as transcriptional coactivators and that their function may be modulated by the GLI proteins and possibly by other cell type-specific cofactors.

* This work was supported by the Special Coordination Fund for Promoting Science and Technology and grants from the Japanese Ministry of Education, Science and Culture, the Takeda Science Foundation, the Naito Foundation, and the Senri Life Science Foundation.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: Developmental Neurobiology Laboratory, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan. Tel.: 81-48-467-9745; Fax: 81-48-467-9744; E-mail: jaruga@brain.riken.go.jp.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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