Norris Rachael P, Freudzon Leon, Freudzon Marina, Hand Arthur R, Mehlmann Lisa M, Jaffe Laurinda A
Department of Cell Biology, University of Connecticut Health Center, Farmington, CT 06032, USA.
Dev Biol. 2007 Oct 15;310(2):240-9. doi: 10.1016/j.ydbio.2007.07.017. Epub 2007 Jul 24.
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.
完全成熟的脊椎动物卵母细胞减数分裂前期阻滞的维持依赖于激活腺苷酸环化酶并提高环磷酸腺苷（cAMP）水平的G(s) G蛋白的活性，在小鼠卵母细胞中，G(s) 由组成型活性孤儿受体GPR3激活。为了确定促黄体生成素（LH）对小鼠卵巢卵泡的作用是否通过抑制GPR3 - G(s) 信号传导导致减数分裂恢复，我们研究了LH对Gα(s) 定位的影响。响应外源性表达的β(2) - 肾上腺素能受体刺激的G(s) 激活会导致Gα(s) 从卵母细胞质膜转移到细胞质中，而响应β(2) - 肾上腺素能受体抑制的G(s) 失活会导致Gα(s) 回到质膜。然而，LH不会引起Gα(s) 定位的变化，表明LH不是通过终止受体 - G(s) 信号传导起作用。
