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Endocrinology Vol. 142, No. 11 4652-4662
Copyright © 2001 by The Endocrine Society

ARTICLES

Unexpected Virilization in Male Mice Lacking Steroid 5{alpha}-Reductase Enzymes

Mala S. Mahendroo, Kristi M. Cala, David L. Hess and David W. Russell

Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, Texas 75390; and Division of Reproductive Sciences, Oregon Regional Primate Research Center (D.L.H.), Beaverton, Oregon 97006

Address all correspondence and requests for reprints to: Dr. David W. Russell, Department of Molecular Genetics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9046. E-mail: russell{at}utsw.swmed.edu

Mice lacking steroid 5{alpha}-reductase 1 and 2 were produced by gene targeting and breeding. Male mice without 5{alpha}-reductase 2 or without both enzymes had fully formed internal and external genitalia and were fertile, but had smaller prostates and seminal vesicles than controls. T accumulated to high levels in the reproductive tissues of the mutant mice. DHT administration increased seminal vesicle and coagulating gland weights in mice deficient in 5{alpha}-reductase 2 and increased the weights of the prostate, seminal vesicle, and coagulating gland in animals deficient in both enzymes. An inhibitor of both 5{alpha}-reductases (GI 208335X) decreased prostate and coagulating gland weights of control mice, but had no effect in those lacking 5{alpha}-reductase 1 and 2. Castration reduced the sizes of these tissues in animals of all genotypes. Androgen-dependent gene expression was decreased in the seminal vesicles of mice lacking one or more 5{alpha}-reductases and was restored by administration of T or DHT. Female mice missing both enzymes exhibited parturition and fecundity defects similar to those of animals without 5{alpha}-reductase 1. We conclude that T is the only androgen required for differentiation of the male urogenital tract in mice and that the synthesis of DHT serves largely as a signal amplification mechanism.




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