Deletion of SNAP-23 results in pre-implantation embryonic lethality in mice.

SNARE-mediated membrane fusion is a pivotal event for a wide-variety of biological processes. SNAP-25, a neuron-specific SNARE protein, has been well-characterized and mouse embryos lacking Snap25 are viable. However, the phenotype of mice lacking SNAP-23, the ubiquitously expressed SNAP-25 homolog,...

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Bibliographic Details
Main Authors: Young Ho Suh, Aki Yoshimoto-Furusawa, Karis A Weih, Lino Tessarollo, Katherine W Roche, Susan Mackem, Paul A Roche
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-03-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3066230?pdf=render
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Summary:SNARE-mediated membrane fusion is a pivotal event for a wide-variety of biological processes. SNAP-25, a neuron-specific SNARE protein, has been well-characterized and mouse embryos lacking Snap25 are viable. However, the phenotype of mice lacking SNAP-23, the ubiquitously expressed SNAP-25 homolog, remains unknown. To reveal the importance of SNAP-23 function in mouse development, we generated Snap23-null mice by homologous recombination. We were unable to obtain newborn SNAP-23-deficient mice, and analysis of pre-implantation embryos from Snap23(Δ/wt) matings revealed that Snap23-null blastocysts were dying prior to implantation at embryonic day E3.5. Thus these data reveal a critical role for SNAP-23 during embryogenesis.
ISSN:1932-6203