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  Two pathways regulate cortical granule translocation to prevent polyspermy in mouse oocytes.

Cheeseman, L. P., Boulanger, J., Bond, L. M., & Schuh, M. (2016). Two pathways regulate cortical granule translocation to prevent polyspermy in mouse oocytes. Nature Communications, 7: 13726. doi:10.1038/ncomms13726.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002C-30AA-5 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002C-30B8-5
Genre: Journal Article

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 Creators:
Cheeseman, L. P., Author
Boulanger, J., Author
Bond, L. M., Author
Schuh, M.1, Author              
Affiliations:
1Department of Meiosis, MPI for Biophysical Chemistry, Max Planck Society, ou_2205654              

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 Abstract: An egg must be fertilized by a single sperm only. To prevent polyspermy, the zona pellucida, a structure that surrounds mammalian eggs, becomes impermeable upon fertilization, preventing the entry of further sperm. The structural changes in the zona upon fertilization are driven by the exocytosis of cortical granules. These translocate from the oocyte’s centre to the plasma membrane during meiosis. However, very little is known about the mechanism of cortical granule translocation. Here we investigate cortical granule transport and dynamics in live mammalian oocytes by using Rab27a as a marker. We show that two separate mechanisms drive their transport: myosin Va-dependent movement along actin filaments, and an unexpected vesicle hitchhiking mechanism by which cortical granules bind to Rab11a vesicles powered by myosin Vb. Inhibiting cortical granule translocation severely impaired the block to sperm entry, suggesting that translocation defects could contribute to miscarriages that are caused by polyspermy.

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Language(s): eng - English
 Dates: 2016-12-19
 Publication Status: Published online
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
 Identifiers: DOI: 10.1038/ncomms13726
 Degree: -

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Title: Nature Communications
Source Genre: Journal
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Pages: 13 Volume / Issue: 7 Sequence Number: 13726 Start / End Page: - Identifier: -