Journal of Andrology
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Published-Ahead-of-Print January 24, 2007, DOI:10.2164/jandrol.106.002006
Journal of Andrology, Vol. 28, No. 3, May/June 2007
Copyright © American Society of Andrology
DOI: 10.2164/jandrol.106.002006

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Abnormal Morphology of Spermatozoa in Cytochrome P450 17{alpha}-hydroxylase/17, 20-lyase (CYP17) Deficient Mice

YING LIU*, LUIS E. DETTIN*, JANET FOLMER{dagger}, BARRY R. ZIRKIN{dagger} AND VASSILIOS PAPADOPOULOS*

From the * Department of Biochemistry & Molecular and Cellular Biology, Georgetown University Medical Center, Washington, DC; and the {dagger} Department of Biochemistry and Molecular Biology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland.

Correspondence to: Dr Vassilios Papadopoulos, Georgetown University Medical Center, Department of Biochemistry & Molecular and Cellular Biology, 3900 Reservoir Road NW, Washington DC, 20057 (e-mail: papadopv{at}georgetown.edu).


Cytochrome P450 17{alpha}-hydroxylase/17, 20-lyase (CYP17) is crucial for cortisol and sex steroid biosynthesis. In a previous study we examined CYP17 function by generating mice with a targeted CYP17 deletion. We found that in addition to its role in steroid biosynthesis, CYP17 is present in germ cells. In the present study we examined the effect of CYP17 on sperm morphology. Disorganization of the sperm midpiece, small sperm mitochondria with reduced inner membranes and matrix, and irregular sperm shape were found to be associated with the CYP17 gene deletion. Treating the mice carrying the CYP17 deletion with testosterone did not alleviate the observed sperm phenotypes, suggesting that CYP17 acts in a testosterone-independent manner. These results suggest that CYP17, in addition to its role in androgen formation, is critical for proper mitochondrial architecture and sperm morphology and thus for sperm function and normal fertility.

     Key words: Gene deletion, steroidogenesis, mitochondria architecture, fertility






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