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G Protein-Coupled Receptor Kinases and Beta Arrestins Are Relocalized and Attenuate Cyclic 3',5'-Adenosine Monophosphate Response to Follicle-Stimulating Hormone in Rat Primary Sertoli Cells¹

^a UMR 6073, INRA/CNRS/Université de Tours, Station de Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France

The FSH receptor (FSH-R) is a member of the rhodopsin-like subfamily of G protein-coupled receptors that undergoes homologous desensitization upon agonist stimulation. In immortalized cell lines overexpressing the FSH-R, G protein-coupled receptor kinases (GRKs) and ß-arrestins are involved in the phosphorylation, uncoupling, and internalization of this receptor. In an effort to appreciate the physiological relevance of GRK/ß-arrestin actions in natural FSH-R-bearing cells, we used primary rat Sertoli cells as a model. GRK2, -3, -5, -6a, and -6b and ß-arrestins 1 and 2 were expressed in primary rat Sertoli cells. Overexpression of these different GRKs and ß-arrestins in primary rat Sertoli cells significantly attenuated the FSH-induced cAMP response, and FSH rapidly triggered a relocalization of endogenously expressed GRK2, -3, -5, and -6 and ß-arrestins 1 and 2 from the cytosol to the membranes. These results highlight the relationship existing between the GRK/ß-arrestin regulatory system and the FSH-R signaling machinery in a physiological model.

First decision: 4 May 2001.

¹ S.M. is the recipient of a doctoral fellowship from the Région Centre-INRA. P.C. is funded by a fellowship from the Fondation d'Aide à la Recherche ORGANON. This work was also funded by the Ligue contre le cancer.

² Correspondence. FAX: 33 2 47427743; reiter{at}tours.inra.fr

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