Beta-glucuronidase activity is present in the microscopic epididymis of the Tfm/Y mouse

The sex-linked recessive gene Tfm in the mouse produces a condition of testicular feminization (androgen insensitivity syndrome, AIS) in hemizygotes, comparable to the condition of the same name in humans. The murine mutant was originally believed to have no derivatives of the mesonephric duct system (MDS), and this absence was ascribed to dependence of these derivatives on androgens for survival. However, microscopical epididymides, retia testes, and vasa deferentia were identified in these animals in our laboratory. These micro-organs may play a role in meiosis induction in Tfm/Y animals. The present study was designed to determine whether survival of these organs is due to retention of an ability to respond to androgens, or whether they are unique amongst MDS derivatives in being independent of androgens. Previous studies in our laboratory demonstrated that the enzyme beta-glucuronidase (beta G) is androgen sensitive in the epididymis of the normal mouse. In the present investigation we used this enzyme as a marker to study androgen sensitivity in the microscopical epididymides of Tfm/Y hemizygotes and in the epididymides of control +/Y litter-mate brothers. Both mutant and control animals were studied with and without exogenous androgen stimulation. Tfm/Y hemizygotes demonstrated low levels of diffuse, cytoplasmic beta G activity that appears to be unresponsive to exogenous androgen stimulation. In light of our previous studies, this distribution of beta G reaction products suggests some degree of androgen sensitivity. The survival of these micro-organs and their partial androgen sensitivity may be related to the role of the MDS in inducing meiosis.