Kuroda H, Terada N, Nakayama H, Matsumoto K, Kitamura Y
Department of Pathology, Osaka University Medical School, Japan.
Dev Biol. 1988 Mar;126(1):71-9. doi: 10.1016/0012-1606(88)90240-0.
Sl, Sld, and Slt are mutant alleles at the steel locus. All Sl/Sld and most Sl/Slt female mice are infertile, but the cause of the infertility is different. Germ cells are absent in Sl/Sld ovaries but present in Sl/Slt ovaries. The infertility of Sl/Slt female mice was attributed to the growth arrest of ovarian follicles, and the mechanism was analyzed by producing aggregation chimeras between Sl/Slt and +/+ embryos. Sl/Slt oocytes were ovulated and fertilized in Sl/Slt----+/+ chimeras. We investigated the origin of granulosa cells in the growing follicles and that of granulosa-derived luteal cells in the chimeras by using the electrophoretic pattern of phosphoglycerate kinase-1 and the histochemical activity of beta-glucuronidase as markers. Granulosa cells of Sl/Slt genotype developed and constituted pregnant corpora lutea in Sl/Slt----+/+ chimeras. Therefore, the growth arrest of Sl/Slt ovarian follicles may not be due to an intrinsic defect in granulosa cells but may instead be due to an intrinsic defect in ovarian stromal cells. This suggests that normal stromal cells are essential for the development of ovarian follicles.
Sl、Sld和Slt是Steel基因座上的突变等位基因。所有Sl/Sld和大多数Sl/Slt雌性小鼠均不育，但不育原因不同。Sl/Sld卵巢中没有生殖细胞，而Sl/Slt卵巢中有生殖细胞。Sl/Slt雌性小鼠的不育归因于卵巢卵泡的生长停滞，通过在Sl/Slt和+/+胚胎之间产生聚集嵌合体来分析其机制。在Sl/Slt-+/+嵌合体中，Sl/Slt卵母细胞排卵并受精。我们使用磷酸甘油酸激酶-1的电泳图谱和β-葡萄糖醛酸酶的组织化学活性作为标记，研究了嵌合体中生长卵泡中颗粒细胞的起源以及颗粒细胞来源的黄体细胞的起源。Sl/Slt基因型的颗粒细胞在Sl/Slt-+/+嵌合体中发育并形成妊娠黄体。因此，Sl/Slt卵巢卵泡的生长停滞可能不是由于颗粒细胞的内在缺陷，而是可能由于卵巢基质细胞的内在缺陷。这表明正常的基质细胞对卵巢卵泡的发育至关重要。
