Figure 2.

Restoration of spermatogenesis in Sl/Sl^d mutant testis transduced by lentiviral-mediated KL2 gene transfer. We prepared lentiviral vector, LV-CMV-KL2, to express membrane type c-kit receptor ligand (KL2). Western blot analysis after lentiviral gene transfer in vitro (a) and in vivo (b). (a) Recombinant KL2 expression was detected in 293T cells at 3 days after transduction (lane 1, untransduced; lane 2, transduced). (b) Recombinant KL2 expression and calmegin (CM) expression were detected in recipient Sl/Sl^d mutant testis at 4 wk after treatment (lane 1, Sl/Sl^d testis; lane 2, Sl/Sl^d testis injected with LV-CMV-KL2). (c) Macroscopic appearance of Sl/Sl^d testis (L) and LV-CMV-KL2 injected Sl/Sl^d testis (R). (d–g) Histological analysis of seminiferous tubules of Sl/Sl^d recipient mouse testes at 2 mo after LV-CMV-KL2 injection. Frozen sections were stained with hematoxylin/eosin (d–f). Sl/Sl^d mutant testis with disrupted spermatogenesis (d). The morphologically normal spermatogenesis occurred in the recipient Sl/Sl^d testis (e and f). The serial section of e was immunostained with anti-calmegin antibody (g). Asterisk indicates the seminiferous tubule in which spermatogenesis was not restored. [Bars = 2 mm (c), 100 μm (d, e, and g), and 20 μm (f).]