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Department of Pediatrics, Yale University New Haven, Connecticut 06510
The National Science Foundation, The George Washington University Washington, D.C. 20550
Laboratories for Reproductive Biology, Department of Pediatrics, University of North Carolina Chapel Hill, North Carolina 27599
Department of Biochemistry, University of North Carolina Chapel Hill, North Carolina 27599
Department of Pathology University of North Carolina Chapel Hill, North Carolina 27599
Address requests for reprints to: Nancy J. Charest, M.D., Department of Pediatrics, Yale University School of Medicine, 333 Cedar Street, P.O. Box 3333, New Haven, Connecticut 06510.
Abstract
A composite mouse androgen receptor DNA sequence was obtained by amplifying genomic DNA or cDNA using the polymerase chain reaction. The open reading frame was 2,697 basepairs, encoding a polypeptide of 899 amino acids (98,204 mol wt). Amino acid sequence comparisons indicated that the mouse androgen receptor (AR) is 97% homologous with rat AR and 83% with human AR. The amino acid sequences of the three receptors are identical within the DNA- and steroid-binding domains. Northern blot analysis revealed the predominant mouse AR mRNA to be 10 kilobases (kb). A 1.7-kb mRNA species was detected in mouse kidney using a cDNA probe containing only 5' untranslated AR sequence. Lack of hybridization with AR-coding sequence probes suggested that the 1.7-kb mRNA was not a truncated form of AR mRNA. Sequencing of genomic DNA isolated from testicular feminized (Tfm) mice revealed a single base deletion in the N-terminal domain, resulting in a frameshift mutation. Cycloheximide treatment caused a dramatic increase in AR mRNA in kidneys of Tfm mice, but not wild-type mice, suggesting that the Tfm mutation results in an unstable AR mRNA.
FOOTNOTES
This work was supported by NIH Grants HD-00756, HD-04466, HD-15221, and P30-HD-18968 (Recombinant DNA Core).
* Genentech Clinical Scholar supported by Genentech, Inc. (South San Francisco, CA).
Supported by the Population Sciences Division of the Rockefeller Foundation.
Supported by the Pew Scholars Program in the Biomedical Sciences.
Received for publication October 30, 1990. Revision received February 6, 1991. Accepted for publication February 12, 1991.
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