Fig. 2

Evidence for involvement of gonadotropin signaling in amh deficiency-induced gonadal hypergrowth and dysfunctional gametogenesis. (A) Ovaries of different genotypes at 5 mpf. The amh single mutation (amh−/−;fshr+/−) caused ovarian hypertrophy with accumulation of PG follicles, whereas the fshr single mutant (amh+/−;fshr−/−) showed ovarian hypotrophy with much fewer, underdeveloped PG follicles only. Double mutation of amh and fshr (amh−/−;fshr−/−) completely abolished the phenotype of amh mutant. (B) Testes of different genotypes at 5 mpf. The amh mutation alone (amh−/−;fshr+/−;lhcgr+/−) caused testicular hypertrophy and dysfunctional spermatogenesis with limited meiosis, whereas the loss of gonadotropin signaling in the fshr and lhcgr double mutant (amh+/−;fshr−/−;lhcgr−/−) led to testicular hypotrophy and dysfunctional spermatogenesis, with no meiosis. The loss of all the three genes in the triple knockout (amh−/−;fshr−/−;lhcgr−/−) completely abolished the hypertrophic phenotype of amh mutation. LV, late vitellogenic; SC, spermatocytes; SG, spermatogonia; SZ, spermatozoa. Arrows indicate ovaries or testes.