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Title
A floxed allele of the androgen receptor gene causes hyperandrogenization in male mice.
Publication Date
2008-01-02
Author(s)
MacLean, Helen E
Chiu, W S Maria
Ma, Cathy
McManus, Julie F
Davey, Rachel A
Cameron, Rhoda
Notini, Amanda J
Zajac, Jeffrey D
Type of document
Journal Article
DOI
10.1152/physiolgenomics.00260.2007
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 (AR(lox)) have the reverse phenotype, termed hyperandrogenization. AR(lox) 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 AR(lox) males are fertile. AR(lox) 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.
Link
Citation
Physiological Genomics 2008; 33(1): 133-7
Jornal Title
Physiological genomics

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