Oocyte-specific deletion of Pten causes premature activation of the primordial follicle pool
Oocyte-specific deletion of Pten causes premature activation of the primordial follicle pool
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DOI：
10.1126/science.1152257
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发表时间：
2008-02-01
期刊：
影响因子：
56.9
通讯作者：
Liu, Kui
中科院分区：
文献类型：
--
作者：
Reddy, Pradeep;Liu, Lian;Liu, Kui
在哺乳动物卵巢中，休眠池中原始卵泡的逐渐激活是可受精卵的来源。更年期，或女性生殖生命的结束，发生在原始卵泡池耗尽时。然而，卵泡激活的分子机制知之甚少。我们提供的遗传证据表明，在卵母细胞中缺乏PTEN（10号染色体上缺失的磷酸酶和张力蛋白同源物）的小鼠中，磷脂酰肌醇3-激酶（PI 3 K）的主要负调节因子，整个原始卵泡池被激活。随后，所有原始卵泡在成年早期耗尽，导致卵巢早衰（POF）。我们的研究结果表明，哺乳动物卵母细胞作为总部的编程卵泡激活和卵母细胞的PTEN-PI 3 K途径管理卵泡激活通过控制卵母细胞生长的启动。
In the mammalian ovary, progressive activation of primordial follicles from the dormant pool serves as the source of fertilizable ova. Menopause, or the end of female reproductive life, occurs when the primordial follicle pool is exhausted. However, the molecular mechanisms underlying follicle activation are poorly understood. We provide genetic evidence that in mice lacking PTEN ( phosphatase and tensin homolog deleted on chromosome 10) in oocytes, a major negative regulator of phosphatidylinositol 3- kinase ( PI3K), the entire primordial follicle pool becomes activated. Subsequently, all primordial follicles become depleted in early adulthood, causing premature ovarian failure ( POF). Our results show that the mammalian oocyte serves as the headquarters of programming of follicle activation and that the oocyte PTEN- PI3K pathway governs follicle activation through control of initiation of oocyte growth.