The alpha and beta chains of follitropin (follicle-stimulating hormone; FSH) and lutropin (luteinizing hormone; LH) have been isolated from the anterior pituitary gland and their cDNAs completely sequenced. The alpha chains are identical; the beta chains differ. The high affinity, non-covalent binding between the alpha and beta subunits leads to the formation of functional heterodimers important for gonadal cell growth and differentiation.
NCBI Summary:
The four human glycoprotein hormones chorionic gonadotropin (CG), luteinizing hormone (LH), follicle stimulating hormone (FSH), and thyroid stimulating hormone (TSH) are dimers consisting of alpha and beta subunits that are associated noncovalently. The alpha subunits of these hormones are identical, however, their beta chains are unique and confer biological specificity. The protein encoded by this gene is the alpha subunit and belongs to the glycoprotein hormones alpha chain family.
General function
Ligand, Hormone
Comment
Cellular localization
Secreted
Comment
Ovarian function
Comment
In addition to the well-established endocrine functions of FSH, recent studies by Markkula et al. (1996) indicated that the common alpha-subunit and the FSH-beta mRNA were detected in the pituitary gland and ovaries of normal adult mice. It was proposed that endogenously synthesized FSH or its subunits may have a role in the paracrine regulation of ovarian function.
Expression regulated by
Comment
Ovarian localization
Luteal cells, Stromal cells
Comment
The cellular localization of the the common alpha-subunit and the FSH-beta proteins was visualized by immunocytochemistry Markkula et al. (1996). In normal mouse ovaries a positive reaction with FSH beta and C alpha antisera was seen in some of the corpora lutea and most prominently in the interstitial cells. It was proposed that endogenously synthesized FSH or its subunits may have a role in the paracrine regulation of ovarian function.
Follicle stages
Comment
Phenotypes
Mutations
1 mutations
Species: mouse
Mutation name: None
type: null mutation fertility: None Comment:Kendall et al. (1995) created a disruption of the alpha-subunit gene by homologous recombination. The homozygous mutant animals were hypogonadal and exhibited profound hypothyroidism resulting in dwarfism. Thyroid development was arrested in late gestation, but GnRH neuron migration, development of secondary sex organs, and fetal and neonatal gonadal development were normal. This establishes the importance of thyrotropin in
ontogeny and reveals that fetal pituitary gonadotropins are not required for sexual differentiation or genital development in male or female fetuses.