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Summary. Cryptorchid testes from adult mice were incubated in calf serum-supplemented medium. There was an effective differentiation of adult type A spermatogonia up to the pachytene stage of meiotic division which resembled the process of spermatogenesis in vivo. In the absence of calf serum, type A spermatogonia did not differentiate at all. They differentiated when the serum was present for the first day, but was absent for the rest of cultivation.
These results indicate that serum is necessary for only the early process of spermatogenesis from type A spermatogonia in vitro and not for the further processes of germ cell differentiation. Type A spermatogonia cultured in serum-free medium retained the ability to differentiate for at least 3 days.
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Summary. The effect of the mutation for white belly spot controlled by the dominant gene W on spermatogenesis in mice was examined by experimental cryptorchidism and its surgical reversal. The course of spermatogenesis from spermatogonia to spermatid was normal in intact testes of W/+ mice. In cryptorchid testes, there was no difference in the number and activity of Type A spermatogonia between the testes of W/+ and +/+ mice, in mitotic and labelling indices. Although surgical reversal of the cryptorchid testis resulted in regenerative differentiation of germ cells in both genotypes, the recovery of cell differentiation in the W/+ testis was slower than in the +/+ testis. There were fewer germ cells, such as intermediate–Type B spermatogonia or more advanced ones, in W/+ testes. On Day 17 after surgical reversal, cell associations in W/+ testes were abnormal and the numbers of intermediate–Type B spermatogonia, spermatocytes and spermatids were approximately ∼70, 50 and 15%, respectively, of those in +/+ testes. These results indicate that the W gene affects spermatogenic cell differentiation in adult mice.
Keywords: W mutation; spermatogenesis; cryptorchidism; orchidopexy; mouse
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Testicular cells composed mostly of germ cells and immature Sertoli cells from neonatal mice 2 and 5 days old were cultured to investigate germ-cell proliferation mediated by the c-kit receptor. The addition of antibody to block the interaction of the c-kit receptor with its ligand inhibited the proliferation of cultured spermatogonia from 5-day-old mice in a dose-dependent manner, but not from that of 2-day-old mice. The addition of anti-c-kit ACK2 monoclonal antibody also inhibited the proliferation of spermatogonia from 5-day-old mutant Sld/Sld mice but not of 5-day-old mutant Wo/Wo mice. The results indicate that c-kit-positive type A spermatogonia in the testes of 5-day-old mice require steel factor (kit ligand) for their proliferation, whereas self-renewal and differentiation of c-kit-negative primitive type A spermatogonia in the testes of 2-day-old mice do not.
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Regulation of steel factor (SF) production in Sertoli cells from postnatal mouse testes was studied in a mast cell–Sertoli cell coculture system. Treatment of Sertoli cells with dibutyryl cAMP (50–1000 μmol l−1), forskolin (1–25 mmol l−1), and cholera toxin (10 μg ml−1) increased SF production, whereas FSH and theophylline had no significant effect. Furthermore, growth factors and testosterone, which would play some roles in spermatogenesis, were also tested, but none of these stimulated SF production. The constitutive production of SF may, rather, reflect the physiological condition of Sertoli cells in vivo.
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Summary. The effects of Steel–Dickie (Sld) mutations on testicular germ cell differentiation were investigated using experimental cryptorchidism and its surgical reversal in mutant, C57BL/6-Sld/+ and wild-type C57BL/6- +/+ mice. In Sld/+ cryptorchid testes the maintenance of undifferentiated type-A spermatogonia was impaired and their numbers decreased. In contrast, the proliferative activity of type-A spermatogonia in the cryptorchid testis of mutant mice appeared normal as judged by their progression through the cell cycle. Surgical reversal of cryptorchidism resulted in regenerative differentiation of mature germ cells in +/+ testes. However, the regenerative differentiation of type-A spermatogonia which remained in Sld/+ cryptorchid testes was strongly impaired, particularly at two steps of cellular differentiation, from type-A spermatogonia to intermediate or type-B spermatogonia and at meiotic division. Furthermore, in mutant mice, no significant recovery of testicular weight was observed after surgical reversal compared with +/+ mice.
Keywords: Sld mutation; testis; germ cell; Sertoli cell; cryptorchidism; mouse
