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. Author manuscript; available in PMC: 2008 Nov 3.
Published in final edited form as: J Biol Chem. 2006 Dec 1;282(7):5026–5036. doi: 10.1074/jbc.M609360200

Figure 1.

Figure 1

Morphological and histological analysis of FKBP52-deficient males. (A) Growth curves of WT and FKBP52-deficient mice; (B) Comparison of adult wild-type and FKBP52-deficient male external genitalia at dorsal (a and b) and ventral surfaces (c and d). Arrows (in b and d) indicate the under-developed foreskin and ectopic urethral opening at the ventral aspect compared to normal morphology in controls (a and c). Histological sections of wild-type (e) and FKBP52-deficient (f) male genitalia. A red arrow indicates ectopic urethral opening at the ventral aspect compared to normal morphology in controls (black arrow in e). (C) Three-dimensional reconstruction of the mouse E18.5 penises. Wire frame images of outer penile skin and urethra of the three FKBP52 genotypes are shown in a, c and e. In b, d and f, the skins had been artificially removed. The glans penis is colored in gold, while the urethral opening is green, corpus cavernosum (cc) is purple, and the closed urethra is blue. Note that the urethral opening persisted throughout the FKBP52-deficient penile shaft, while normal controls only have a temporary urethral opening at distal end. Side panels show representative sections of wild-type and mutant penises. Green arrows indicate open urethra, blue arrows indicate closed urethra. (D) Comparison of anogenital distances in wild-type, heterozygous and FKBP52-deficient mice. The anogenital distance, normalized by the animal body weight, in FKBP52-deficient males was significantly shorter compared to littermate wild-type and heterozygous males.