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Mol Cell Biol, May 1998, p. 2949-2956, Vol. 18, No. 5
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Nuclear Receptor DAX-1 Recruits Nuclear Receptor Corepressor N-CoR to Steroidogenic Factor 1

Peter A. Crawford,1 Christoph Dorn,2 Yoel Sadovsky,2 and Jeffrey Milbrandt1,*

Departments of Pathology and Internal Medicine1 and Department of Obstetrics and Gynecology,2 Washington University School of Medicine, St. Louis, Missouri 63110

Received 1 December 1997/Returned for modification 26 January 1998/Accepted 13 February 1998

The orphan nuclear receptor steroidogenic factor 1 (SF-1) is a critical developmental regulator in the urogenital ridge, because mice targeted for disruption of the SF-1 gene lack adrenal glands and gonads. SF-1 was recently shown to interact with DAX-1, another orphan receptor whose tissue distribution overlaps that of SF-1. Naturally occurring loss-of-function mutations of the DAX-1 gene cause the human disorder X-linked adrenal hypoplasia congenita (AHC), which resembles the phenotype of SF-1-deficient mice. Paradoxically, however, DAX-1 represses the transcriptional activity of SF-1, and AHC mutants of DAX-1 lose repression function. To further investigate these findings, we characterized the interaction between SF-1 and DAX-1 and found that their interaction indeed occurs through a repressive domain within the carboxy terminus of SF-1. Furthermore, we demonstrate that DAX-1 recruits the nuclear receptor corepressor N-CoR to SF-1, whereas naturally occurring AHC mutations of DAX-1 permit the SF-1-DAX-1 interaction, but markedly diminish corepressor recruitment. Finally, the interaction between DAX-1 and N-CoR shares similarities with that of the nuclear receptor RevErb and N-CoR, because the related corepressor SMRT was not efficiently recruited by DAX-1. Therefore, DAX-1 can serve as an adapter molecule that recruits nuclear receptor corepressors to DNA-bound nuclear receptors like SF-1, thereby extending the range of corepressor action.

* Corresponding author. Mailing address: Department of Pathology and Internal Medicine, Washington University School of Medicine, 660 S. Euclid Ave., Box 8118, St. Louis, MO 63110. Phone: (314) 362-4650. Fax: (314) 362-8756. E-mail: jeff{at}milbrandt.wustl.edu.

Mol Cell Biol, May 1998, p. 2949-2956, Vol. 18, No. 5
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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