Analysis Tools
mortality/aging
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• homozygotes die in utero between E9.5 and E10.5
• a small number (1.3%) survive beyond E10.5 but die at ~E13.5-E14.5 of unknown causes
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embryo
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• at E9.5, ~33.3% of mutant embryos are normal; however, nearly all embryos appear abnormal at E10.5, with extensive necrosis both in the embryo proper and yolk sac
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• at E9.5, severely affected homozygotes display extensive embryonic tissue necrosis
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• at E9.5, homozygotes exhibit wasting of variable onset and penetrance
• ensuing necrosis appears to result from ischemia secondary to defective vitello-embryonic circulation and wasting
• severely affected homozygotes display extensive embryonic tissue necrosis
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• at E9.5, ~66.6% of homozygotes display abnormal yolk sac vessels with strands of acellular material connecting endoderm and mesothelium
• vascular yolk-sac defects precede embryo wasting and necrosis and are noted in embryos still embedded in their decidua
• at E9.5, fragility of mutant vitelline vessels is associated with lack of mesenchymal cell/pericyte accumulation and function, reduced extracellular matrix, and hypoplasia of the muscular wall of primitive vessels; in contrast, endoderm, endothelial and mesothelial cells appear normal
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• at E9.5, ~66.6% of mutant yolk sacs lack large vitelline vessels
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• at E9.5, ~66.6% of homozygotes exhibit an irregular vascular plexus of enlarged capillaries that appear to fuse with each other
• in vitro, cultured E9.5 mutant embryos exhibit a confluent disorganized vascular plexus ("blood lakes") with no large vitelline vessels
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pale yolk sac
(
J:35120
)
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• at E9.5, no blood flow is observed in mutant yolk sacs
• in vitro, cultured E9.5 mutant embryos exhibit pale yolk sacs
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cardiovascular system
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• at E9.5, ~66.6% of homozygotes display abnormal yolk sac vessels with strands of acellular material connecting endoderm and mesothelium
• vascular yolk-sac defects precede embryo wasting and necrosis and are noted in embryos still embedded in their decidua
• at E9.5, fragility of mutant vitelline vessels is associated with lack of mesenchymal cell/pericyte accumulation and function, reduced extracellular matrix, and hypoplasia of the muscular wall of primitive vessels; in contrast, endoderm, endothelial and mesothelial cells appear normal
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• at E9.5, ~66.6% of mutant yolk sacs lack large vitelline vessels
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• at E9.5, ~66.6% of homozygotes exhibit an irregular vascular plexus of enlarged capillaries that appear to fuse with each other
• in vitro, cultured E9.5 mutant embryos exhibit a confluent disorganized vascular plexus ("blood lakes") with no large vitelline vessels
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• in vitro, severely affected E9.5 mutant embryos exhibit an enlarged pericardial sac and blood in the extracoelomic cavity
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integument
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• at E9.5, severely affected homozygotes appear pale and anemic due to extravasation of embryonic blood cells in the extracoelomic cavity
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cellular
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• at E9.5, homozygotes exhibit wasting of variable onset and penetrance
• ensuing necrosis appears to result from ischemia secondary to defective vitello-embryonic circulation and wasting
• severely affected homozygotes display extensive embryonic tissue necrosis
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