PLoS ONE (Mar 2011)

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

  • Young Ho Suh,
  • Aki Yoshimoto-Furusawa,
  • Karis A Weih,
  • Lino Tessarollo,
  • Katherine W Roche,
  • Susan Mackem,
  • Paul A Roche

DOI
https://doi.org/10.1371/journal.pone.0018444
Journal volume & issue
Vol. 6, no. 3
p. e18444

Abstract

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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.