[Hormonal regulation of the expression of genes coding for pituitary gonadotropins]

In the rat, gonadectomy increases and injection of estradiol or of testosterone depresses the translational capacity of mRNAs encoding gonadotropin subunits alpha, LH beta and FSH beta. This inhibitory effect of steroids can also be demonstrated in vitro using pituitary cells in culture. Thus, steroids appear to regulate gonadotropin synthesis, at least in part, by a direct action on the pituitary gland. Hybridization experiments, using labeled cDNA probes, show gonadal steroids to act by decreasing the number of copies of specific mRNAs encoding each one of the gonadotropin subunits. Definite evidence has been obtained that GnRH stimulates biosynthesis of the polypeptide chains of LH subunits, thus confirming our previous observations. Preliminary results suggest cAMP could be involved in this process as a mediator of GnRH action. Although actinomycin D prevents the stimulatory effect of GnRH on gonadotropin biosynthesis, the translational capacity of specific mRNAs encoding LH subunits did not increase after incubation of the cells with GnRH, thus suggesting that GnRH does not act directly either on the gonadotropin subunit genes or on the intrinsic messenger activity of mRNAs encoding the gonadotropin subunit precursors. Our data demonstrate that the synthesis of pituitary gonadotropins is under a dual hormonal control, by gonadal steroids and GnRH. We suggest that the negative control by steroids and stimulatory effect of GnRH occur via different routes, the former at the genomic level, the latter at another step which remains to be elucidated.