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J. Biol. Chem., Vol. 280, Issue 42, 35228-35237, October 21, 2005

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The Optimedin Gene Is a Downstream Target of Pax6^*

Oleg Grinchuk, Zbynek Kozmik, Xiaofang Wu, and Stanislav Tomarev1

From the Section of Molecular Mechanisms of Glaucoma, Laboratory of Molecular and Developmental Biology, NEI, National Institutes of Health, Bethesda, Maryland 20892-0704 and the Institute of Molecular Genetics, 14220 Prague, Czech Republic

The Optimedin gene, also known as Olfactomedin 3, encodes an olfactomedin domain-containing protein. There are two major splice variants of the Optimedin mRNA, Optimedin A and Optimedin B, transcribed from different promoters. The expression pattern of the Optimedin A variant in the eye and brain overlaps with that for Pax6, which encodes a protein containing the paired and homeobox DNA-binding domains. The Pax6 gene plays a critical role for the development of eyes, central nervous system, and endocrine glands. The proximal promoter of the Optimedin A variant contains a putative Pax6 binding site in position –86/–70. Pax6 binds this site through the paired domain in vitro as judged by electrophoretic mobility shift assay. Mutations in this site eliminate Pax6 binding as well as stimulation of the Optimedin promoter activity by Pax6 in transfection experiments. Pax6 occupies the binding site in the proximal promoter in vivo as demonstrated by the chromatin immunoprecipitation assay. Altogether these results identify the Optimedin gene as a downstream target regulated by Pax6. Although the function of optimedin is still not clear, it is suggested to be involved in cell-cell adhesion and cell attachment to the extracellular matrix. Pax6 regulation of Optimedin in the eye and brain may directly affect multiple developmental processes, including cell migration and axon growth.

Received for publication, June 7, 2005 , and in revised form, August 18, 2005.

^* This work was supported by the NEI, National Institutes of Health Intramural Program and by Grant Agency of Czech Republic Grant 204/04/1358 (to Z. K.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Bldg. 7, Rm. 103, 7 Memorial Dr., MSC 0704, Bethesda, MD 20892-0704. Tel.: 301-496-8524; Fax: 301-496-8760; E-mail: tomarevs{at}nei.nih.gov.

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