spacer gif spacer gif spacer gif spacer gif spacer gif
 QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents    

First published online 15 August 2007
doi: 10.1242/dev.005454


Development 134, 3307-3315 (2007)
Published by The Company of Biologists 2007


This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
dev.005454v1
134/18/3307    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by El-Jouni, W.
Right arrow Articles by Machaca, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by El-Jouni, W.
Right arrow Articles by Machaca, K.

Vesicular traffic at the cell membrane regulates oocyte meiotic arrest

Wassim El-Jouni, Shirley Haun, Rawad Hodeify, Azida Hosein Walker and Khaled Machaca*

Department of Physiology and Biophysics, University of Arkansas for Medical Sciences (UAMS), Little Rock, AR 72205, USA.

* Author for correspondence (e-mail: kamachaca{at}uams.edu)

Accepted 13 July 2007

Vertebrate oocytes are maintained in meiotic arrest for prolonged periods of time before undergoing oocyte maturation in preparation for fertilization. Cyclic AMP (cAMP) signaling plays a crucial role in maintaining meiotic arrest, which is released by a species-specific hormonal signal. Evidence in both frog and mouse argues that meiotic arrest is maintained by a constitutively active G-protein coupled receptor (GPCR) leading to high cAMP levels. Because activated GPCRs are typically targeted for endocytosis as part of the signal desensitization pathway, we were interested in determining the role of trafficking at the cell membrane in maintaining meiotic arrest. Here we show that blocking exocytosis, using a dominant-negative SNAP25 mutant in Xenopus oocytes, releases meiotic arrest independently of progesterone. Oocyte maturation in response to the exocytic block induces the MAPK and Cdc25C signaling cascades, leading to MPF activation, germinal vesicle breakdown and arrest at metaphase of meiosis II with a normal bipolar spindle. It thus replicates all tested aspects of physiological maturation. Furthermore, inhibiting clathrin-mediated endocytosis hinders the effectiveness of progesterone in releasing meiotic arrest. These data show that vesicular traffic at the cell membrane is crucial in maintaining meiotic arrest in vertebrates, and support the argument for active recycling of a constitutively active GPCR at the cell membrane.

Key words: Meiotic arrest, Oocyte maturation, Xenopus laevis, Exocytosis, Endocytosis, Clathrin, SNAP25




This article has been cited by other articles:


Home page
J. Cell Sci.Home page
W. El-Jouni, S. Haun, R. Hodeify, A. H. Walker, and K. Machaca
Vesicular traffic at the cell membrane regulates oocyte meiotic arrest
J. Cell Sci., September 15, 2007; 120(18): e1806 - e1806.
[Full Text]




© The Company of Biologists Ltd 2007