Analysis Tools
mortality/aging
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• dead (asystolic) homozygotes are first detected at E10.0; no homozygotes survive beyond E11.0
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cardiovascular system
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• at E9.75-E10.0, homozygotes exhibit only a sparse network of small vessels, with massively enlarged endothelial-lined vascular structures predominantly in the cephalic region, and along the path of dorsal aortae
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• by E9.75, all homozygotes show abnormalities in the diameter and/or position of the intersomitic vessels
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• homozygotes display proper vascularization at E8.5 but exhibit enlarged vascular structures and absence of normal cephalic vascularization by E9.25
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• at E9.25, mutant dorsal aortae exhibit aberrant morphology with localized regions of dilatation
• by E9.75, all homozygotes show abnormalities in the diameter and/or position of the dorsal aortae
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• localized regions of dilatation at E9.25
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• by E9.25, mutant branchial arch vessels are either severely hypoplastic or absent
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• by E9.25, mutant branchial arch vessels are either severely hypoplastic or absent
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• at E9.75-E10.0, homozygotes display hyperplasia of the presumptive myocardium
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• at E9.75, homozygotes exhibit a highly disorganized presumptive myocardium, with as many as 12 concentric cell layers in some regions relative to the 2-3 cell layers found in wild-type
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• 21% of E9.25 and 40% of E9.75 homozygotes exhibit a significantly reduced outflow tract
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• at E9.75, mutant heart tubes show absence of a patent lumen
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• at E9.75-E10.0, homozygotes exhibit enlarged pericardial cavity
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• at E9.75-E10.0, homozygotes display abnormal endothelial-lined vascular structures within the enlarged pericardial cavity and along the pericardium
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• by E10.0, homozygotes display pericardial effusion
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embryo
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• by E9.25, mutant branchial arch vessels are either severely hypoplastic or absent
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• by E9.25, mutant branchial arch vessels are either severely hypoplastic or absent
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• homozygotes begin to display a developmental arrest late at E8, with striking differences noted by E10.0
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• at E9.75-E10.0, homozygotes display extensive mesenchymal cell death in the cranial region, leading to an open neural tube
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• by E10.0, homozygotes exhibit failure of neural tube closure with cystic degeneration and prolapse of the neural folds
• prolapse of the lateral neural folds is associated with buckling of the somatic ectoderm ventral to the neurosomatic junction
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• at E9.75-E10.0, wild-type embryos have a mean of 29 somites, whereas homozygous mutant embryos have a mean of 12 somites
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nervous system
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• by E10.0, homozygotes exhibit failure of neural tube closure with cystic degeneration and prolapse of the neural folds
• prolapse of the lateral neural folds is associated with buckling of the somatic ectoderm ventral to the neurosomatic junction
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• by E10.0, homozygotes display cystic enlargement of the hindbrain
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craniofacial
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• by E9.25, mutant branchial arch vessels are either severely hypoplastic or absent
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• by E9.25, mutant branchial arch vessels are either severely hypoplastic or absent
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cellular
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• at E8.5, homozygotes exhibit excessive cell death prior to the onset of any vascular defects (not shown)
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homeostasis/metabolism
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• by E10.0, homozygotes display pericardial effusion
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growth/size/body
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• at E9.75-E10.0, homozygotes display extensive mesenchymal cell death in the cranial region, leading to an open neural tube
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muscle
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• at E9.75-E10.0, homozygotes display hyperplasia of the presumptive myocardium
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• at E9.75, homozygotes exhibit a highly disorganized presumptive myocardium, with as many as 12 concentric cell layers in some regions relative to the 2-3 cell layers found in wild-type
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