SNAP-23 的缺失导致小鼠胚胎着床前死亡。
Deletion of SNAP-23 results in pre-implantation embryonic lethality in mice.
机构信息
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
出版信息
PLoS One. 2011 Mar 29;6(3):e18444. doi: 10.1371/journal.pone.0018444.
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.
摘要
SNARE 介导的膜融合是多种生物过程的关键事件。SNAP-25 是一种神经元特异性 SNARE 蛋白，其特性已得到充分研究，而缺乏 Snap25 的小鼠胚胎仍然具有活力。然而，缺乏普遍表达的 SNAP-25 同源物 SNAP-23 的小鼠表型仍不清楚。为了揭示 SNAP-23 功能在小鼠发育中的重要性，我们通过同源重组生成了 Snap23 基因敲除小鼠。我们无法获得新生的 SNAP-23 缺失小鼠，而且对 Snap23(Δ/wt)交配的胚胎前植入期的分析表明，在胚胎第 3.5 天之前，SNAP-23 缺失的囊胚在植入前就已经死亡。因此，这些数据揭示了 SNAP-23 在胚胎发生过程中的关键作用。
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