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J. Biol. Chem., Vol. 278, Issue 29, 26572-26579, July 18, 2003
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Gene*
¶
From the
Departments of Molecular and Integrative
Physiology and Internal Medicine, Division of
Endocrinology and Metabolism, University of Michigan, Ann Arbor, Michigan
48109
The action of a variety of peptide hormones is critical for proper growth
and differentiation of the urogenital ridge, which ultimately gives rise to
the kidney, adrenal cortex, and gonad. One such class of peptides is the Wnt
family of secreted glycoproteins that is classically involved in development
of cell polarity and cell fate determination. Notably, alterations in Wnt-4
expression in mice and humans result in profound defects in urogenital ridge
development, including dysregulation of kidney, gonadal, and adrenal growth.
The nuclear receptor steroidogenic factor-1 (SF-1) has been implicated as a
downstream effector of peptide hormone signaling during urogenital ridge
development as evidenced by both the activation of SF-1-dependent
transcription in the adrenal cortex by signaling molecules such as protein
kinase A and by the adrenal and gonadal agenesis in mice with null mutations
in SF-1. We hypothesized that Wnt-dependent signaling cascades regulate
SF-1-dependent transcription of genes required for adreno-gonadal development.
Specifically, the data demonstrate that 
-catenin synergizes with SF-1 to
activate the 
-inhibin promoter through formation of a transcriptional
complex. The activation requires an intact SF-1 RE and is independent of
TCF/Lef. These data support the recent observation that -catenin can
participate in nuclear receptor-mediated transcriptional activation and extend
the findings to the monomer binding class of orphan nuclear receptors.
Received for publication, December 12, 2002 , and in revised form, April 8, 2003.
* This work was supported by National Institutes of Health Grant DK 02393 and a University of Michigan Comprehensive Cancer Center Schembechlar Adrenal Cancer Research Grant (to G. D. H.). 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.
¶ To whom correspondence should be addressed: Dept. of Internal Medicine, Division of Endocrinology and Metabolism, University of Michigan, 1150 W. Medical Center Dr., 5560 MSRBII, Ann Arbor, MI 48109. Tel.: 734-763-3056; Fax: 734-936-6684; E-mail: ghammer{at}umich.edu.
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