[Frontiers in Bioscience 1, d266-269, September 1, 1996]
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CREM: A TRANSCRIPTIONAL MASTER SWITCH DURING THE SPERMATOGENESIS DIFFERENTIATION PROGRAM

François Nantel and Paolo Sassone-Corsi

Institut de Génétique et de Biologie Moléculaire et Cellulaire, 1 rue Laurent Fries, BP 163, ILLKIRCH Cedex, C.U. de Strasbourg, France

Received 08/17/96; Accepted 08/21/96; On-line 09/01/96

3. HORMONAL CONTROL OF TESTICULAR FUNCTION: THE cAMP PATHWAY

The gonadotropin releasing hormone (GnRH) released by the hypothalamus stimulates the secretion of follicule stimulating hormone (FSH) and luteinizing hormones (LH) from the gonadotroph cells of the anterior pituitary (1-3). Receptors for FSH and LH are present on somatic Leydig and Sertoli cells, respectively, which have the function of transmitting the hormonal stimulus to the germ cells (4, 5). The cAMP pathway plays a critical role in this hormonal cascade. When binding of FSH and LH to their respective receptors occurs, it activates their coupling to Gs proteins and stimulates the enzyme adenylyl cyclase which catalyses the conversion of ATP to cAMP. Elevations in intracellular levels of cAMP stimulate the protein kinase A (PKA) which then phosphorylates several substrate proteins. Among the targets of PKA are transcription factors that recognize the cAMP-responsive element (CRE) sequence located on the promoter of many genes. Phosphorylation of these CRE-binding proteins by PKA activates them and drives cAMP-dependent gene expression (6).

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