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Departments of Reproductive Medicine and Neuroscience and The Center for Molecular Genetics University of California, San Diego La Jolla, California 92093-0674
The neuropeptide GnRH is a central regulator of
mammalian reproductive function produced by a dispersed population of
hypothalamic neurosecretory neurons. The principal action of GnRH is to
regulate release of the gonadotropins, LH and FSH, by the gonadotrope
cells of the anterior pituitary. Using a cultured cell model of mouse
pituitary gonadotrope cells, 
T3–1 cells, we present evidence that
GnRH stimulation of T3–1 cells results in an increase in
cap-dependent mRNA translation. GnRH receptor activation results in
increased protein synthesis through a regulator of mRNA translation
initiation, eukaryotic translation initiation factor 4E-binding
protein, known as 4EBP or PHAS (protein, heat, and acid stable).
Although the GnRH receptor is a member of the rhodopsin-like family of
G protein-linked receptors, we show that activation of translation
proceeds through a signaling pathway previously described for receptor
tyrosine kinases. Stimulation of translation by GnRH is protein
kinase C and Ras dependent and sensitive to rapamycin. Furthermore,
GnRH may also regulate the cell cycle in T3–1 cells. The activation
of a signaling pathway that regulates both protein synthesis and cell
cycle suggests that GnRH may have a significant role in the maintenance
of the pituitary gonadotrope population in addition to directing
the release of gonadotropins.
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