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G Protein Autocrine Regulation of Gonadotropin Expression

, : G Protein Autocrine Regulation of Gonadotropin Expression.

Gonadotropin-releasing hormone (GnRH) acts at gonadotropes to direct the synthesis of the gonadotropins, follicle-stimulating hormone (FSH), and luteinizing hormone (LH). The frequency of GnRH pulses determines the pattern of gonadotropin synthesis. Several hypotheses for how the gonadotrope decodes GnRH frequency to regulate gonadotropin subunit genes differentially have been proposed. However, key regulators and underlying mechanisms remain uncertain. We investigated the role of individual G proteins by perturbations using siRNA or bacterial toxins. In L?T2 gonadotrope cells, FSH? gene induction depended predominantly on G?q/11, whereas LH? expression depended on G?s. Specifically reducing G?s signaling also disinhibited FSH? expression, suggesting the presence of a G?s-dependent signal that suppressed FSH biosynthesis. The presence of secreted factors influencing FSH? expression levels was tested by studying the effects of conditioned media from G?s knockdown and cholera toxin-treated cells on FSH? expression. These studies and related Transwell culture experiments implicate G?s-dependent secreted factors in regulating both FSH? and LH? gene expression. siRNA studies identify inhibin? as a G?s-dependent GnRH-induced autocrine regulatory factor that contributes to feedback suppression of FSH? expression. These results uncover differential regulation of the gonadotropin genes by G?q/11 and by G?s and implicate autocrine and gonadotrope-gonadotrope paracrine regulatory loops in the differential induction of gonadotropin genes.


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