Cografting of hamster (Phodopus sungorus) and marmoset (Callithrix jacchus) testicular tissues into nude mice does not overcome blockade of early spermatogenic differentiation in primate grafts.

The ectopic xenotransplantation of testicular tissues into nude mice is a tool to generate sperm from immature testes. Immunodeficient mice as recipients of xenografts offered an appropriate microenvironment for differentiation of testicular tissue from hamsters, goats, pigs, and macaques. One exception is the neotropical primate Callithrix jacchus. Spermatogenesis in testicular grafts from marmosets does not proceed beyond the spermatogonial stage. The most likely cause for the poor graft development of marmosets is a deletion of exon 10 in the luteinizing hormone-receptor (LHR) gene, which renders this species insensitive to LH but responsive to chorionic gonadotropin (CG). We investigated whether cografting of testicular tissue from Djungarian hamsters would overcome the blockade in marmoset graft development. We also tested if exogenous administration of human CG (hCG) to the recipient would stimulate development of the marmoset tissue. No difference in graft survival was noted between hamster and monkey tissue. Seminiferous lumina were present in marmoset and hamster grafts but were significantly larger in hamster grafts. In the hamster grafts, a high proportion of the tubules contained meiotic and postmeiotic germ cells. In contrast, the marmoset tubules were populated with gonocytes and premeiotic spermatogonia. These results indicate that neither normal serum androgen levels nor the high local testosterone levels were sufficient to initiate marmoset spermatogenesis, nor was administration of hCG successful in overcoming the developmental blockade in marmoset tissue. Our results indicate that the conditions needed for initiation of spermatogenesis in the marmoset are remarkably different from those present in most other mammals.