Figure 6: The absence of SIX6OS1 provokes azoospermia and ovarian failure.

(a) Genetic ablation of Six6os1 leads to a reduction of the testis size (n=8 wild-type and knock out, Welch’s t-test analysis: P<0.0001), and (b) a complete arrest of spermatogenesis in epithelial stage IV as shown in hematoxylin-eosin stained testis sections. Massive apoptosis of spermatocytes is indicated (asterisks). The spermatogenic arrest leads to empty epididymides and azoospermia. Scale bar in upper panels, 100 μm and in lower panels, 5 μm. (St) Seminiferous tubules. (Ep) Epididymides. (c) Tubule degeneration in juvenile mice (13 d.p.p. and 18 d.p.p.) lacking SIX6OS1 and spermatogenic arrest before pachytene studied by histology. At 13 d.p.p. spermatogenesis has reached late zygotene; at 18 d.p.p. it has reached late pachytene. Spermatocyte degeneration (apoptosis is indicated by asterisks) was first seen in 18 d.p.p. Six6os1^−/−. (d) Ovaries from Six6os1-deficient mice show atrophy with fibrosis and depletion of follicles. Comparative histological analysis of ovaries from Six6os1^−/− and wild-type mice at 6 days (6 d.p.p.), and 4 months (4 m) of age. Asterisks indicate corpora lutea. Scale bars represent 100 μm in 4 m, and 20 μm in 6 d.p.p.