Deletion of SNAP-23 results in pre-implantation embryonic lethality in mice.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 21479242.
- Also identified by DOI 10.1371/journal.pone.0018444 and PMC identifier 3066230.
- Licence recorded as CC0.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
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.
Medical subject headings
- Embryo Implantation
- Embryo Loss
- Gene Deletion
- Qb-SNARE Proteins
- Qc-SNARE Proteins