Abstract
Follicle–stimulating hormone (FSH) is a pituitary-derived gonadotropin that plays key roles in male and female reproduction. The physiology and biochemistry of FSH have been extensively studied for many years. Beginning in the early 1990s, coincident with advances in the then emerging transgenic animal technology, and continuing till today, several gain-of-function (GOF) models have been developed to understand FSH homeostasis in a physiological context. Our group and others have generated a number of FSH ligand and receptor GOF mouse models. An FSH GOF model when combined with Fshb null mice provides a powerful genetic rescue platform. In this chapter, we discuss different GOF models for FSH synthesis, secretion and action and describe additional novel genetic models that could be developed in the future to further refine the existing models.
Highlights
Follicle–Stimulating Hormone (FSH) is a gonadotropin synthesized in gonadotropes of the anterior pituitary gland
Co-localization of mutant FSHβ and Chr-A was higher when compared to both control and Fshb null mice expressing a HFSHBWT transgene and was similar to levels seen with co-localization of LHβ (37)
These results suggest that the engineered mutant FSHβ- containing FSH heterodimer successfully entered the regulated secretory pathway
Summary
Follicle–Stimulating Hormone (FSH) is a gonadotropin synthesized in gonadotropes of the anterior pituitary gland. Low- level ectopic expression of HFSHB was achieved in multiple tissues using a mouse metallothionein (mMT-1) gene promoter with the goal of genetically restoring reproductive phenotypes in FSH-deficient mice, designated as type 2 rescue (FR-II) (36). The results with the type 2 genetic rescue suggest that ectopic expression of human FSH can completely rescue Fshb null male mice, yet only partially rescue Fshb null females (36).
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