Regulation of meiotic prophase arrest in mouse oocytes by GPR3, a constitutive activator of the Gs G protein

Author:

Freudzon Leon1,Norris Rachael P.1,Hand Arthur R.2,Tanaka Shigeru3,Saeki Yoshinaga3,Jones Teresa L.Z.4,Rasenick Mark M.56,Berlot Catherine H.7,Mehlmann Lisa M.1,Jaffe Laurinda A.1

Affiliation:

1. Department of Cell Biology, University of Connecticut Health Center, Farmington, CT 06032

2. Department of Pediatric Dentistry, University of Connecticut Health Center, Farmington, CT 06032

3. Department of Neurological Surgery, The Ohio State University, Columbus, OH 43210

4. National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892

5. Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL 60612

6. Department of Psychiatry, University of Illinois at Chicago, Chicago, IL 60612

7. Weis Center for Research, Geisinger Clinic, Danville, PA 17822

Abstract

The arrest of meiotic prophase in mouse oocytes within antral follicles requires the G protein Gs and an orphan member of the G protein–coupled receptor family, GPR3. To determine whether GPR3 activates Gs, the localization of Gαs in follicle-enclosed oocytes from Gpr3+/+ and Gpr3−/− mice was compared by using immunofluorescence and GαsGFP. GPR3 decreased the ratio of Gαs in the oocyte plasma membrane versus the cytoplasm and also decreased the amount of Gαs in the oocyte. Both of these properties indicate that GPR3 activates Gs. The follicle cells around the oocyte are also necessary to keep the oocyte in prophase, suggesting that they might activate GPR3. However, GPR3-dependent Gs activity was similar in follicle-enclosed and follicle-free oocytes. Thus, the maintenance of prophase arrest depends on the constitutive activity of GPR3 in the oocyte, and the follicle cell signal acts by a means other than increasing GPR3 activity.

Publisher

Rockefeller University Press

Subject

Cell Biology

Cited by 84 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3