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Sci. STKE, 4 September 2007 EDITORS' CHOICEMeiosis Vesicular Trafficking in Meiotic ArrestNancy R. Gough Science's STKE, AAAS, Washington, DC 20005, USA
A constitutively active G protein-coupled receptor (GPCR) resulting in the production of adenosine 3',5'-monophosphate (cAMP) has been implicated in maintaining meiotic arrest. El-Jouni et al. investigated whether vesicular trafficking at the plasma membrane may be involved in this process. Using Xenopus oocytes, they inhibited exocytosis with a dominant-negative form of SNAP25 (a protein that functions as a critical component of the SNARE machinery that allows vesicles to fuse with the plasma membrane) and found that the oocytes were released from meiotic arrest in the absence of hormonal stimulation (progesterone). Membrane capacitance was monitored as an indicator of exocytosis. Forskolin, which directly activates adenylyl cyclase in the absence of receptor stimulation, and cholera toxin, which activates G W. El-Jouni, S. Haun, R. Hodeify, A. H. Walker, K. Machaca, Vesicular traffic at the cell membrane regulates oocyte meiotic arrest. Development 134, 3307-3315 (2007). [PubMed]
Citation: N. R. Gough, Vesicular Trafficking in Meiotic Arrest. Sci. STKE 2007, tw319 (2007). The editors suggest the following Related Resources on Science sites:In Science Signaling
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Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882