A Gs-linked receptor maintains meiotic arrest in mouse oocytes, but luteinizing hormone does not cause meiotic resumption by terminating receptor-Gs signaling

• DOI: 10.1016/j.ydbio.2007.07.017
• Publication Date: 2007-07-25T11:18:23Z
• Authors: Rachael P. Norris; Leon Freudzon; Marina Freudzon; Arthur R. Hand; Lisa M. Mehlmann; Laurinda A. Jaffe
• Keywords: Luteinizing hormone; 0301 basic medicine; Mouse; Follicle-enclosed oocytes; In Vitro Techniques; Receptors, G-Protein-Coupled; Mice; 03 medical and health sciences; Meiotic resumption; Oocyte maturation; GTP-Binding Protein alpha Subunits, Gs; Animals; Molecular Biology; Cells, Cultured; Crosses, Genetic; Cell Membrane; Cell Biology; Luteinizing Hormone; Mice, Inbred C57BL; Meiosis; Protein Transport; Heterotrimeric G proteins; Oocytes; Female; Receptors, Adrenergic, beta-2; Developmental Biology; Signal Transduction

The maintenance of meiotic prophase arrest in fully grown vertebrate oocytes depends on the activity of a G(s) G-protein that activates adenylyl cyclase and elevates cAMP, and in the mouse oocyte, G(s) is activated by a constitutively active orphan receptor, GPR3. To determine whether the action of luteinizing hormone (LH) on the mouse ovarian follicle causes meiotic resumption by inhibiting GPR3-G(s) signaling, we examined the effect of LH on the localization of Galpha(s). G(s) activation in response to stimulation of an exogenously expressed beta(2)-adrenergic receptor causes Galpha(s) to move from the oocyte plasma membrane into the cytoplasm, whereas G(s) inactivation in response to inhibition of the beta(2)-adrenergic receptor causes Galpha(s) to move back to the plasma membrane. However, LH does not cause a change in Galpha(s) localization, indicating that LH does not act by terminating receptor-G(s) signaling.