Figure 7.

Infertility in Rb cKO mice may be caused by abnormal expression of genes important to tight junction formation and tissue remodeling. A, Venn diagram of changes in AR-related, cell adhesion molecules (CAMs) and tight junctions (TJs), and proteases and their inhibitors shows the overlap between these pathways. B, Quantitative RT-PCR of select (bold) genes from panel A and Ar confirms the misregulation of these genes in Rb cKO Sertoli cells (*, P < 0.05; **, P < 0.01; control, n = 6; Rb cKO, n = 5). RQ, Relative quantification. C and E, A biotin tracer (red) was injected into 6-wk-old control (C) and Rb cKO (E) testes. Presence of biotin in the adluminal space of the Rb cKO mice indicates that these mice have a defect in blood-testis barrier function. C–F, Espin (green) marks the basal ectoplasmic specializations (white arrows) of the blood-testis barrier. The normal curvilinear staining of the basal ectoplasmic specializations in the control (D) has been lost in Rb cKO (F). The insets show the proximity between the blood-testis barriers and the basement membranes (dashed line). Espin also marks the apical ectoplasmic specializations (red arrows) that are important for formation of the sperm head, and this staining is neither organized nor polarized in Rb cKO (F) as they are in the control (D).