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Male Reproductive Defects Caused by Puromycin-Sensitive Aminopeptidase Deficiency in Mice

Mitsubishi Kasei Institute of Life Sciences (T.O., S.K., M.T., T.T.) Tokyo,194–8511, Japan
Laboratory of Functional Genomics (T.O., Y.S.) Human Genome Center The Institute of Medical Science University of Tokyo Tokyo 108-8639, Japan.
Laboratory of Veterinary Physiology (G.W.) Tokyo University of Agriculture and Technology Tokyo 183-8509, Japan

Male reproductive performance is composed of two principal elements, copulation and spermatogenesis. A wealth of literature has described the intricate web of endocrine events underlying these biological processes. In the present study we show that puromycin-sensitive aminopeptidase (Psa)-deficient mice are infertile, lack copulatory behavior, and have impaired spermatogenesis. The reproductive deficits of the mutants are not restored by androgen administration, although no aberrant localization of the sex steroid receptors was detectable in their brains and testes. Considering the strong expression of the Psa gene in the brain and Sertoli cells and the degenerative morphology of Sertoli cells in Psa-deficient mice, Psa may participate in testosterone-mediated reproductive signal pathways in the brain and testis.

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