[HTML][HTML] Epiblast-specific Snai1 deletion results in embryonic lethality due to multiple vascular defects
H Lomelí, C Starling, T Gridley - BMC research notes, 2009 - Springer
H Lomelí, C Starling, T Gridley
BMC research notes, 2009•SpringerAbstract 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 …
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 …
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.
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