Lomelí Hilda, Starling Christa, Gridley Thomas
Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma deMéxico, Cuernavaca, Morelos, México.
BMC Res Notes. 2009 Feb 6;2:22. doi: 10.1186/1756-0500-2-22.
Members of the Snail gene family, which encode zinc finger proteins that function as transcriptional repressors, play essential roles during embryonic development in vertebrates. Mouse embryos with conditional deletion of the Snail1 (Snai1) gene in the epiblast, but not in most extraembryonic membranes, exhibit defects in left-right asymmetry specification and migration of mesoderm cells through the posterior primitive streak. Here we describe phenotypic defects that result in death of the mutant embryos by 9.5 days of gestation.
Endothelial cells differentiated in epiblast-specific Snai1-deficient embryos, but formation of an interconnected vascular network was abnormal. To determine whether the observed vascular defects were dependent on disruption of blood flow, we analyzed vascular remodeling in cultured allantois explants from the mutant embryos. Similar vascular defects were observed in the mutant allantois explants.
These studies demonstrate that lethality in the Snai1-conditional mutant embryos is caused by multiple defects in the cardiovascular system.
Snail基因家族的成员编码作为转录抑制因子发挥作用的锌指蛋白，在脊椎动物胚胎发育过程中起重要作用。在胚泡而非大多数胚外膜中条件性缺失Snail1（Snai1）基因的小鼠胚胎，在左右不对称性确定以及中胚层细胞通过后原条迁移方面表现出缺陷。在此我们描述了导致突变胚胎在妊娠9.5天时死亡的表型缺陷。
在胚泡特异性Snai1缺陷胚胎中分化出了内皮细胞，但相互连接的血管网络形成异常。为了确定观察到的血管缺陷是否依赖于血流中断，我们分析了来自突变胚胎的培养尿囊外植体中的血管重塑。在突变尿囊外植体中观察到了类似的血管缺陷。
这些研究表明，Snai1条件性突变胚胎中的致死性是由心血管系统的多种缺陷引起的。
