Choi Youngsok, Yuan Daniel, Rajkovic Aleksandar
Fertility Center of CHA General Hospital, CHA Research Institute, Pochon CHA University, Seoul 135-081, Republic of Korea.
Biol Reprod. 2008 Dec;79(6):1176-82. doi: 10.1095/biolreprod.108.071217. Epub 2008 Aug 27.
We previously discovered a germ cell-specific spermatogenesis and oogenesis basic helix-loop-helix transcription factor, Sohlh2. We generated Sohlh2-deficient mice to understand physiologic consequences of Sohlh2 deletion. We discovered that Sohlh2-knockout adult female mice are infertile due to lack of ovarian follicles. Sohlh2-deficient ovaries can form primordial follicles and, despite limited oocyte growth, do not differentiate surrounding granulosa cells into cuboidal and multilayered structures. Oocytes are rapidly lost in Sohlh2-deficient ovaries, and few are present by 14 days of postnatal life. However, the primordial oocytes are abnormal at the molecular level because they misexpress numerous germ cell- and oocyte-specific genes, including Sohlh1, Nobox, Figla, Gdf9, Pou5f1, Zp1, Zp3, Kit, Oosp1, Nlrp14, H1foo, and Stra8. Our findings show that Sohlh2 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis.
我们之前发现了一种生殖细胞特异性的生精和卵子发生碱性螺旋-环-螺旋转录因子，即Sohlh2。我们构建了Sohlh2基因缺失的小鼠，以了解Sohlh2缺失的生理后果。我们发现，Sohlh2基因敲除的成年雌性小鼠由于缺乏卵巢卵泡而不育。Sohlh2基因缺失的卵巢能够形成原始卵泡，尽管卵母细胞生长有限，但不能将周围的颗粒细胞分化为立方形和多层结构。卵母细胞在Sohlh2基因缺失的卵巢中迅速丢失，出生后14天时几乎所剩无几。然而，原始卵母细胞在分子水平上是异常的，因为它们错误表达了许多生殖细胞和卵母细胞特异性基因，包括Sohlh1、Nobox、Figla、Gdf9、Pou5f1、Zp1、Zp3、Kit、Oosp1、Nlrp14、H1foo和Stra8。我们的研究结果表明，Sohlh2是早期卵子发生过程中卵母细胞维持和分化的关键因子。
