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

Dev Biol. 2007 Oct 15;310(2):240-9. doi: 10.1016/j.ydbio.2007.07.017. Epub 2007 Jul 24.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cell Membrane / metabolism
  • Cells, Cultured
  • Crosses, Genetic
  • Female
  • GTP-Binding Protein alpha Subunits, Gs / physiology*
  • In Vitro Techniques
  • Luteinizing Hormone / pharmacology*
  • Meiosis / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Oocytes / drug effects
  • Oocytes / physiology*
  • Protein Transport
  • Receptors, Adrenergic, beta-2 / metabolism
  • Receptors, G-Protein-Coupled / agonists
  • Receptors, G-Protein-Coupled / physiology*
  • Signal Transduction

Substances

  • GPR3 protein, mouse
  • Receptors, Adrenergic, beta-2
  • Receptors, G-Protein-Coupled
  • Luteinizing Hormone
  • GTP-Binding Protein alpha Subunits, Gs