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The glycoprotein FSH, a product of pituitary gonadotrope cells, regulates ovarian follicle development in females and spermatogenesis in males. Deletion of Foxl2 or Smad4 alone led to FSH deficiency, female subfertility, and oligozoospermia in males.
Simultaneous deletion of the two genes yielded a greater suppression of FSH and female sterility. The Cre-driver used previously was first active during embryonic development. To address this question, we developed a tamoxifen-inducible Cre-driver line, which enabled Foxl2 and Smad4 gene deletions in gonadotropes of adult mice. After tamoxifen treatment, females with previously demonstrated fertility exhibited profound reductions in FSH levels, arrested ovarian follicle development, and sterility.
FSH levels were comparably reduced in males 1 or 2 months after treatment; however, spermatogenesis was unaffected. These data indicate that 1 FOXL2 and SMAD4 are necessary to maintain FSH synthesis in gonadotrope cells of adult mice, 2 FSH is essential for female reproduction but appears to be unnecessary for the maintenance of spermatogenesis in adult male mice, and 3 the inducible Cre-driver line developed here provides a powerful tool to interrogate gene function in gonadotrope cells of adult mice.
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Alexandre Boyer. Chu-Xia Deng. Mathias Treier. Ulrich Boehm. Derek Boerboom. Daniel J Bernard. E-mail: daniel. Cite Citation. Permissions Icon Permissions. Abstract The glycoprotein FSH, a product of pituitary gonadotrope cells, regulates ovarian follicle development in females and spermatogenesis in males. Issue Section:. Download all figures. View Metrics. Email alerts Article activity alert. Advance article alerts. New issue alert. In progress issue alert. Receive exclusive offers and updates from Oxford Academic.