Anti-Müllerian hormone (AMH/Amh) plays a role in gonadal differentiation and function across vertebrates. In zebrafish we demonstrated that Amh deficiency caused severe gonadal dysgenesis and dysfunction. The mutant gonads showed extreme hypertrophy with accumulation of early germ cells in both sexes, namely spermatogonia in the testis and primary growth oocytes in the ovary. In amh mutant females, the folliculogenesis was normal in young fish but receded progressively in adults, which was accompanied by progressive decrease in follicle-stimulating hormone (fshb) expression. Interestingly the expression of fshb increased in the pituitary of juvenile amh mutant males but decreased in adults. The upregulation of fshb in mutant male juveniles was likely one of the mechanisms for triggering gonadal hypergrowth, whereas the downregulation of fshb in adults might involve a negative feedback by gonadal inhibin. Further analysis using mutants of fshb and growth differentiation factor 9 (gdf9) provided evidence for a role of FSH in triggering ovarian hypertrophy in young female amh mutant as well. In summary, the present study provided comprehensive genetic evidence for dual roles of Amh in controlling zebrafish gonadal homeostasis and gametogenesis in both sexes. Amh suppresses proliferation or accumulation of early germ cells (spermatogonia in testis and primary growth oocytes in ovary) while promoting their exit to advanced stages, and its action may involve both endocrine and paracrine pathways.

抗苗勒管激素（AMH / Amh）在脊椎动物的性腺分化和功能中发挥作用。在斑马鱼中，我们证明了Amh缺乏会导致严重的性腺发育不全和功能障碍。突变的性腺表现出极度肥大，男女都有早期生殖细胞的积累，即睾丸中的精原细胞增多，卵巢中的原代卵母细胞增多。在amh突变雌性中，幼鱼的卵泡形成是正常的，而在成年鱼中则逐渐下降，这伴随着卵泡刺激素（fshb）表达的逐渐下降。有趣的是，fshb的表达在幼年的amh突变型雄性垂体中增加，而在成年中则降低。fshb的上调在突变的雄性少年中，可能是触发性腺过度生长的机制之一，而成人中fshb的下调可能涉及性腺抑制素的负反馈。使用fshb和生长分化因子9（gdf9）突变体的进一步分析提供了FSH在触发年轻女性amh卵巢肥大中的作用的证据。突变体也是如此。总而言之，本研究为Amh在控制斑马鱼性腺稳态和配子发生中的双重作用提供了全面的遗传证据。Amh抑制早期生殖细胞（睾丸中的精原细胞和卵巢中的原代卵母细胞）的增殖或积累，同时促进其退出晚期，其作用可能涉及内分泌和旁分泌途径。