Cited by 32Developmental Biology and Gene RegulationCongenital heart defects researchZebrafish Biomedical Research Applications

Epiblast-specific Snai1 deletion results in embryonic lethality due to multiple vascular defects

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Lomelí, Hilda, Starling, Christa, Gridley, Thomas·2009·BMC Research Notes

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.

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Authors
Lomelí, H., Starling, C., & Gridley, T.
Affiliations
Jackson Laboratory (US)
Corresponding author
Gridley, Thomas
Venue
BMC Research Notes
Published
2009
Volume
2
Issue
1
Pages
22
ISSN
1756-0500 (ISSN-L)
OpenAlex
W2085181221
Cited by
32
References
27
Citations by year
2025: 3 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 3 · 2018: 2 · 2016: 2 · 2015: 3 · 2014: 4 · 2013: 2 · 2012: 6
FWCI
1.21
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • BMC Research Notes (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion, cc-by)
Funders
  • National Institutes of Health (CA 034196)
  • Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México
  • National Cancer Institute (P30CA034196)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD034883)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Zebrafish Biomedical Research Applications
Keywords
SNAI1, epiblast, conditional gene deletion, embryonic lethality, vascular defects, endothelial differentiation, vascular network formation, cardiovascular development, left-right asymmetry, mesoderm migration, transcriptional repressor

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