Analysis Tools
mortality/aging
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• homozygous mutant embryos die at E9.5-E10.5; abnormal or necrotic embryos appear with increasing frequency from E10.5 to E11.5
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embryo
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• at E9.5, mutant placentas contain fewer embryonic vessels, and the vessels fail to invade deep into the labyrinth layer; reduced intermingling of maternal and embryonic blood vessels is observed
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• at E9.5, mutant yolk sacs exhibit thinner, poorly defined vessels containing fewer red blood cells
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• at E9.5, the large collecting vessels present in wild-type yolk sacs are nearly absent in mutant embryos
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• although homozygotes exhibit a normal size at E8.5, they appear smaller at E9.5 probably as a result of vascular and cardiac developmental defects
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pale yolk sac
(
J:77725
)
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• at E9.5, mutant yolk sacs are generally pale
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• homozygotes display failure of the vascular plexus to remodel into a mature vascular network
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cardiovascular system
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• at E9.5, the endothelial cells lining the mutant myocardium appear rounded and disorganized relative to the thin, elongated cells present in the wild-type
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• at E9.5, mutant placentas contain fewer embryonic vessels, and the vessels fail to invade deep into the labyrinth layer; reduced intermingling of maternal and embryonic blood vessels is observed
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• at E9.5, homozygotes display defective vascular pruning/maturation resulting in a disorganized vascular network
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• at E9.5, the mutant dorsal aorta and branchial arteries exhibit reduced smooth muscle cell investment relative to wild-type embryonic vessels
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• at E9.5, mutant vessels fail to show complex branching in the head region, indicating defective vascular maturation
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• at E9.5, mutants exhibit normal intersomitic vessels but lack the angiogenic pruning and remodeling that is present in the head region of wild-type embryos
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• at E9.5, mutant yolk sacs exhibit thinner, poorly defined vessels containing fewer red blood cells
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• at E9.5, the large collecting vessels present in wild-type yolk sacs are nearly absent in mutant embryos
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• at E9.5, the mutant dorsal aorta and branchial arteries exhibit reduced smooth muscle cell investment relative to wild-type embryonic vessels
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• at E9.5, homozygotes display underdeveloped and disorganized ventricular trabeculations
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• at E9.5, homozygotes display delayed cardiac development with an enlarged common atrial chamber
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• at E9.5, mutant hearts fail to undergo normal rightward looping
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• at E9.5, homozygotes display retarded development of the right ventricle
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• at E9.5, homozygotes exhibit excessive pericardial edema, suggesting hemodynamic insufficiency
• consistent with pericardial fluid accumulation, mutants display a large space between the heart and pericardium
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growth/size/body
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• although homozygotes exhibit a normal size at E8.5, they appear smaller at E9.5 probably as a result of vascular and cardiac developmental defects
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homeostasis/metabolism
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• at E9.5, homozygotes exhibit excessive pericardial edema, suggesting hemodynamic insufficiency
• consistent with pericardial fluid accumulation, mutants display a large space between the heart and pericardium
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muscle
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• at E9.5, the mutant dorsal aorta and branchial arteries exhibit reduced smooth muscle cell investment relative to wild-type embryonic vessels
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• at E9.5, homozygotes display underdeveloped and disorganized ventricular trabeculations
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