Physiol. Genomics AJP: Endocrinology and Metabolism
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Physiol. Genomics 33: 133-137, 2008. First published January 2, 2008; doi:10.1152/physiolgenomics.00260.2007
1094-8341/08 $8.00
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Received 6 November 2007; accepted in final form 28 December 2007.
Physiological Genomics 33:133-137 (2008)
1094-8341/08 $8.00 © 2008 American Physiological Society

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A floxed allele of the androgen receptor gene causes hyperandrogenization in male mice

Helen E. MacLean1, W. S. Maria Chiu1, Cathy Ma1, Julie F. McManus1, Rachel A. Davey1, Rhoda Cameron2, Amanda J. Notini1 and Jeffrey D. Zajac1

1 Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria, Australia
2 Department of Anatomical Pathology, Austin Health, Heidelberg, Victoria, Australia

ABSTRACT

We previously generated a conditional floxed mouse line to study androgen action, in which exon 3 of the androgen receptor (AR) gene is flanked by loxP sites, with the neomycin resistance gene present in intron 3. Deletion of exon 3 in global AR knockout mice causes androgen insensitivity syndrome, characterized by genotypic males lacking normal masculinization. We now report that male mice carrying the floxed allele (ARlox) have the reverse phenotype, termed hyperandrogenization. ARlox mice have increased mass of androgen-dependent tissues, including kidney, (P < 0.001), seminal vesicle (P < 0.001), levator ani muscle (P = 0.001), and heart (P < 0.05). Serum testosterone is not significantly different. Testis mass is normal, histology shows normal spermatogenesis, and ARlox males are fertile. ARlox males also have normal AR mRNA levels in kidney, brain, levator ani, liver, and testis. This study reaffirms the need to investigate the potential phenotypic effects of floxed alleles in the absence of cre in tissue-specific knockout studies. In addition, this androgen hypersensitivity model may be useful to further investigate the effects of subtle perturbations of androgen action in a range of androgen-responsive systems in the male.

androgen; testosterone; cre/lox; hypomorphic allele; androgen insensitivity






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