Epiblast-specific Snai1 deletion results in embryonic lethality due to multiple vascular defects.
Document Type
Article
Publication Date
2009
First Page
22
Last Page
22
JAX Source
BMC Res Notes 2009; 2:22.
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. FINDINGS: 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. CONCLUSION: These studies demonstrate that lethality in the Snai1-conditional mutant embryos is caused by multiple defects in the cardiovascular system.
Recommended Citation
Lomeli H,
Starling C,
Gridley T.
Epiblast-specific Snai1 deletion results in embryonic lethality due to multiple vascular defects. BMC Res Notes 2009; 2:22.