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

The maintenance of meiotic prophase arrest in fully grown vertebrate oocytes depends on the activity of a Gs G-protein that activates adenylyl cyclase and elevates cAMP, and in the mouse oocyte, Gs is activated by a constitutively active orphan receptor, GPR3. To determine whether the action of lute...

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Bibliographic Details
Published in:Developmental biology 2007-10, Vol.310 (2), p.240-249
Main Authors: Norris, Rachael P., Freudzon, Leon, Freudzon, Marina, Hand, Arthur R., Mehlmann, Lisa M., Jaffe, Laurinda A.
Format: Article
Language:English
Subjects:
Follicle-enclosed oocytes
Heterotrimeric G proteins
Luteinizing hormone
Meiotic resumption
Mouse
Oocyte maturation
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Summary:The maintenance of meiotic prophase arrest in fully grown vertebrate oocytes depends on the activity of a Gs G-protein that activates adenylyl cyclase and elevates cAMP, and in the mouse oocyte, Gs 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-Gs signaling, we examined the effect of LH on the localization of Gαs. Gs activation in response to stimulation of an exogenously expressed β2-adrenergic receptor causes Gαs to move from the oocyte plasma membrane into the cytoplasm, whereas Gs inactivation in response to inhibition of the β2-adrenergic receptor causes Gαs to move back to the plasma membrane. However, LH does not cause a change in Gαs localization, indicating that LH does not act by terminating receptor-Gs signaling.
ISSN:0012-1606
1095-564X
DOI:10.1016/j.ydbio.2007.07.017