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Originally published In Press as doi:10.1074/jbc.M206796200 on October 3, 2002

J. Biol. Chem., Vol. 277, Issue 51, 49903-49910, December 20, 2002
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MafA Is a Glucose-regulated and Pancreatic beta -Cell-specific Transcriptional Activator for the Insulin Gene*

Kohsuke KataokaDagger §, Song-iee HanDagger , Setsuko ShiodaDagger , Momoki Hirai, Makoto Nishizawa||, and Hiroshi HandaDagger

From the Dagger  Frontier Collaborative Research Center, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama 226-8503, Japan, the  Department of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, Tokyo 277-8562, Japan, and the || Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, California 92037

The insulin gene is specifically expressed in beta -cells of the Langerhans islets of the pancreas, and its transcription is regulated by the circulating glucose level. Previous reports have shown that an unidentified beta -cell-specific nuclear factor binds to a conserved cis-regulatory element called RIPE3b and is critical for its glucose-regulated expression. Based on the sequence similarity of the RIPE3b element and the consensus binding sequence of the Maf family of basic leucine zipper transcription factors, we here identified mammalian homologue of avian MafA/L-Maf, an eye-specific member of the Maf family, as the RIPE3b-binding transcriptional activator. Reverse transcription-PCR analysis showed that mafA mRNA is detected only in the eyes and in pancreatic beta -cells and not in alpha -cells. MafA protein as well as its mRNA is up-regulated by glucose, consistent with the glucose-regulated binding of MafA to the RIPE3b element in beta -cell nuclear extracts. In transient luciferase assays, we also showed that expression of MafA greatly enhanced insulin promoter activity and that a dominant-negative form of MafA inhibited it. Therefore, MafA is a beta -cell-specific and glucose-regulated transcriptional activator for insulin gene expression and thus may be involved in the function and development of beta -cells as well as in the pathogenesis of diabetes.

* This work was supported by Grants-in-Aid for Scientific Research on Priority Areas and for Encouragement of Young Scientists from the Ministry of Education, Science, Sports and Culture in Japan and a grant from the Ministry of Health, Labor and Welfare in Japan (to K. K.).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: Frontier Collaborative Research Center, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama 226-8503, Japan. Tel.: 81-45-924-5799; Fax: 81-45-924-5834; E-mail: kkataoka@bio.titech.ac.jp.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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