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Infertility due to growth arrest of ovarian follicles in Sl/Slt mice
H Kuroda1, N Terada, H Nakayama
1Department of Pathology, Osaka University Medical School, Japan.
Abstract:
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.
Insights
Female mice with Sl/Slt mutations are infertile due to ovarian follicle growth arrest. This infertility stems from ovarian stromal cell defects, not granulosa cell issues, highlighting stromal cell importance in follicle development.
Area of Science:
- Reproductive biology
- Developmental biology
- Genetics
Background:
- Mutant alleles Sl, Sld, and Slt at the steel locus affect female mouse fertility.
- Sl/Sld and Sl/Slt female mice exhibit infertility with distinct ovarian pathologies.
- Sl/Slt infertility is linked to ovarian follicle growth arrest, despite the presence of germ cells.
Purpose of the Study:
- To elucidate the mechanism behind ovarian follicle growth arrest in Sl/Slt female mice.
- To determine the cellular origin of the defect causing infertility in Sl/Slt mice.
- To investigate the role of granulosa and stromal cells in ovarian follicle development.
Main Methods:
- Production of aggregation chimeras between Sl/Slt and wild-type (+/+) embryos.
- Utilizing electrophoretic patterns of phosphoglycerate kinase-1 as a genetic marker.
- Employing histochemical activity of beta-glucuronidase to trace cell lineages.
- Analyzing the origin of granulosa cells and granulosa-derived luteal cells in chimeric ovaries.
Main Results:
- Sl/Slt oocytes were successfully ovulated and fertilized in Sl/Slt----+/+ chimeras.
- Granulosa cells of Sl/Slt genotype developed and formed pregnant corpora lutea in chimeric ovaries.
- The findings indicate that Sl/Slt granulosa cells are not intrinsically defective.
Conclusions:
- The growth arrest of ovarian follicles in Sl/Slt mice is likely caused by an intrinsic defect in ovarian stromal cells.
- Normal ovarian stromal cells are essential for the proper development of ovarian follicles.
- This study redefines the cellular basis of infertility associated with steel locus mutations.