Building pathways for ovary organogenesis in the mouse embryo.
Building pathways for ovary organogenesis in the mouse embryo.
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DOI：
10.1016/s0070-2153(10)90007-0
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发表时间：
2010
影响因子：
--
通讯作者：
Yao, Humphrey H-C
中科院分区：
文献类型：
--
作者：
Liu, Chia-Feng;Liu, Chang;Yao, Humphrey H-C
尽管卵巢在成年期的卵母细胞生成和激素产生中起着重要作用，但与男性睾丸相比，卵巢的形成很少受到关注。除了生殖细胞经历雌性特有的减数分裂模式外，胎儿卵巢的形态变化是微妙的。在过去的40年里，已经提出了许多关于哺乳动物卵巢器官发生的假说。直到千禧年之交，由于遗传和基因组方法的进步，由阳性和阴性调节剂组成的卵巢器官发生途径才开始出现。通过分泌因子（R-spondin 1，WNT 4和卵泡抑素）和转录调节因子（β-连环蛋白和FOXL 2）的作用，体细胞的发育命运被导向卵巢，而睾丸成分被抑制。在这一章中，我们回顾了研究哺乳动物卵巢器官发生的历史，并介绍了最新的发现使用小鼠作为模式生物。
Despite its significant role in oocyte generation and hormone production in adulthood, the ovary, with regard to its formation, has received little attention compared to its male counterpart, the testis. With the exception of germ cells, which undergo a female-specific pattern of meiosis, morphological changes in the fetal ovary are subtle. Over the past 40 years, a number of hypotheses have been proposed for the organogenesis of the mammalian ovary. It was not until the turn of the millennium, thanks to the advancement of genetic and genomic approaches, that pathways for ovary organogenesis that consist of positive and negative regulators have started to emerge. Through the action of secreted factors (R-spondin1, WNT4, and follistatin) and transcription regulators (β-catenin and FOXL2), the developmental fate of the somatic cells is directed toward ovarian, while testicular components are suppressed. In this chapter, we review the history of studying ovary organogenesis in mammals and present the most recent discoveries using the mouse as the model organism.