title: Epiblast-specific Snai1 deletion results in embryonic lethality due to multiple vascular defects.
abstract: BACKGROUND
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  These studies demonstrate that lethality in the Snai1-conditional mutant embryos is caused by multiple defects in the cardiovascular system.
authors.affiliation: Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma deMéxico, Cuernavaca, Morelos, México. hilda@ibt.unam.mx
authors.forename: Hilda
authors.initials: H
authors.lastname: Lomelí
authors.forename: Christa
authors.initials: C
authors.lastname: Starling
authors.forename: Thomas
authors.initials: T
authors.lastname: Gridley