FGF9 promotes survival of germ cells in the fetal testis
FGF9 promotes survival of germ cells in the fetal testis
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DOI：
10.1242/dev.02303
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发表时间：
2006-04-15
期刊：
影响因子：
4.6
通讯作者：
Capel, B
中科院分区：
文献类型：
--
作者：
DiNapoli, L;Batchvarov, J;Capel, B
除了其在睾丸体细胞发育中的作用外，我们的数据还揭示了Fgf 9在XY生殖细胞存活中的作用。在Fgf 9基因敲除小鼠中，XY性腺中的生殖细胞数量在交配后11.5天（dpc）后下降，而XX性腺中的生殖细胞数量不受影响。我们目前的证据表明，生殖细胞在XY性腺成为依赖于FGF 9信号之间的10.5 dpc和11.5 dpc，和FGF 9直接促进XY生殖细胞存活后11.5 dpc，独立于支持细胞分化。此外，XY Fgf 9-null性腺经历真正的雄性到雌性的性逆转，因为它们启动但不能维持雄性途径，随后表达卵巢分化的标志物（Fst和Bmp 2）。到14.5 dpc，这些性腺含有生殖细胞，与卵巢生殖细胞同步进入减数分裂。FGF 9是11.5 dpc XY生殖细胞存活所必需的，并且是最早报道的在调节生殖细胞存活中具有asex特异性作用的因子。
In addition to its role in somatic cell development in the testis, our data have revealed a role for Fgf9 in XY germ cell survival. In Fgf9-null mice, germ cells in the XY gonad decline in numbers after 11.5 days post coitum (dpc), while germ cell numbers in XX gonads are unaffected. We present evidence that germ cells resident in the XY gonad become dependent on FGF9 signaling between 10.5 dpc and 11.5 dpc, and that FGF9 directly promotes XY gonocyte survival after 11.5 dpc, independently from Sertoli cell differentiation. Furthermore, XY Fgf9-null gonads undergo true male-to-female sex reversal as they initiate but fail to maintain the male pathway and subsequently express markers of ovarian differentiation (Fst and Bmp2). By 14.5 dpc, these gonads contain germ cells that enter meiosis synchronously with ovarian gonocytes. FGF9 is necessary for 11.5 dpc XY gonocyte survival and is the earliest reported factor with asex-specific role in regulating germ cell survival.