Male-to-female sex reversal in mice lacking fibroblast growth factor 9
Male-to-female sex reversal in mice lacking fibroblast growth factor 9
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DOI：
10.1016/s0092-8674(01)00284-7
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发表时间：
2001-03-23
期刊：
影响因子：
64.5
通讯作者：
Ornitz, DM
中科院分区：
文献类型：
--
作者：
Colvin, JS;Green, RP;Ornitz, DM
纤维生长因子指导包括肺、肢体和垂体前叶在内的几个器官的胚胎发生。在这里，我们报告了缺乏成纤维细胞生长因子9（FGF 9）的小鼠的雄性到雌性的性逆转，证明了FGF信号在睾丸胚胎发生中的新作用。Fgf 9（/-）小鼠也表现出肺发育不全并在出生时死亡。生殖系统表型的范围从睾丸发育不全到完全性逆转，大多数Fgf 9（-/-）生殖系统在出生时表现为女性。Fgf 9似乎在Sly的下游起作用，以刺激胚胎睾丸中的间充质增殖、中肾细胞迁移和支持细胞分化。虽然Sry仅在一些哺乳动物中发现，但Fgf是高度保守的。因此，Fgfs可能在许多物种的性别决定和生殖系统发育中发挥作用。
Fgfs direct embryogenesis of several organs, including the lung, limb, and anterior pituitary. Here we report male-to-female sex reversal in mice lacking Fibroblast growth factor 9 (Fgf9), demonstrating a novel role for FGF signaling in testicular embryogenesis. Fgf9(/-) mice also exhibit lung hypoplasia and die at birth. Reproductive system phenotypes range from testicular hypoplasia to complete sex reversal, with most Fgf9(-/-) reproductive systems appearing grossly female at birth. Fgf9 appears to act downstream of Sly to stimulate mesenchymal proliferation, mesonephric cell migration, and Sertoli cell differentiation in the embryonic testis. While Sry is found only in some mammals, Fgfs are highly conserved. Thus, Fgfs may function in sex determination and reproductive system development in many species.