Inability of Tfm (testicular feminization) epithelial cells to express androgen-dependent seminal vesicle secretory proteins in chimeric tissue recombinants.

To assess the role of androgen receptors (ARs) in the expression of androgen-dependent seminal vesicle (SV) secretory proteins, tissue recombinants were prepared with rat seminal vesicle mesenchyme plus ureter epithelium of wild-type or Tfm mice (rat SVM plus wild-type mouse URE and rat SVM plus Tfm mouse URE, respectively). After growth in male hosts, both the wild-type and Tfm ureter epithelia were induced by SVM to differentiate into a simple columnar epithelium exhibiting the complex folded morphology characteristic of the SV. In SVM plus wild-type mouse URE recombinants, epithelial ARs were induced, and the epithelium expressed the full spectrum of SV secretory proteins. By contrast, in SVM plus Tfm mouse URE recombinants, the Tfm epithelium was genetically incapable of producing functional ARs and failed to produce SV secretory proteins. These data demonstrate in vivo that the induction of SV secretory proteins by androgens is an event requiring intraepithelial ARs. In contrast, androgen-dependent epithelial morphogenesis, columnar cytodifferentiation, and probably also proliferation can be expressed in Tfm epithelium grown in association with wild-type mesenchyme, strongly suggesting that these events are indirect effects on the epithelium mediated by mesenchymal ARs.