Analysis Tools
mortality/aging
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• none of the mice survive more than 1 day after birth due to complex cardiovascular malformations
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• some lethality occurs during embryonic and fetal development with significantly less homozygous embryos observed than expected between E11.5 and E12.5 (21 observed when 37.5 expected), and between E15.0 and E16.5 (25 observed when 40 expected)
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vision/eye
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• in all fetuses, eyelids do not fuse together
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growth/size/body
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• cleft palate is first observed in E14.5 embryos
• is observed in 42.9% of embryos between E16.5-E18.5
• is observed in 28.1% of neonates
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omphalocele
(
J:141306
)
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• omphalocele is first observed in E13.5 embryos
• is observed in 53.6% of embryos between E16.5-E18.5
• is observed in 25% of neonates
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nervous system
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• E9.5 embryos have excessive apoptosis in the hindbrain region and in adjacent craniofacial tissues
• there is a 2-fold increase in apoptosis of the mesenchymal cells
• there is also a 2-fold increase in apoptosis of the neuorepithelial cells of the E9.5 rostral hindbrain, and a 3-fold increase in the caudal hindbrain
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• at E9.5, about 42% of embryos exhibit a cranial neural tube closure defect (NTD) in the form of exencephaly
• exencephalic embryos show failed bending of the neural folds at the dorsolateral hinge point
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• in the 58% of embryos that are not exencephalic, the telencephalic roof plate is malformed
• roof plate strucutures including the cortical hem, dorsal hippocampal primordium, and the choroid plexus are either hypomorphic or missing
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• everted at E14.5
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• at E14.5, non-exencephalic embryos have enlarged brain ventricles
a
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• at E14.5, exencephalic embryos show a severely malformed brain in the hindbrain region
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• everted at E14.5
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anencephaly
(
J:141306
)
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• by birth, exencephalic mutants have only rudimentary brain tissue left, resembling that of human anencephaly
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exencephaly
(
J:141306
)
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• at E9.5, about 42% of mice exhibit exencephaly i.e., brain tissue exposed
without bony covering
• skull and the skin overlying the brain are absent in these embryos at E14.5
• by E14.5 both tel and diencephalon are identifiable in exencephalic brains, but they are severely compressed by the everted hindbrain structures
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cardiovascular system
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• 17.0% of E16.5 to neonates have double outlet of the right ventricles (DORV) that contributes to the animals death
• 5.1% of embryos have both DORV and ventricular septum defects
• 3.3% of embryos have both DORV and transposition of great arteries
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• 30.5% of E16.5 to neonates have transposition of the great arteries that contributes to the animals death
• 3.3% of embryos have both double outlet of the right ventricles and transposition of great arteries
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• 35.6 % of E16.5-neonates have ventral septum defects
• 5.1% of embryos have both double outlet of the right ventricles and ventricular septum defects
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craniofacial
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• cleft palate is first observed in E14.5 embryos
• is observed in 42.9% of embryos between E16.5-E18.5
• is observed in 28.1% of neonates
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homeostasis/metabolism
embryo
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• at E9.5, exencephalic embryos show failed bending of the neural folds toward the dorsal midline in the midbrain and hindbrain region
• the dorsolateral folds are convex instead of concave due to a failure of bending at the dorsolateral hinge
• in contrast, the medial hinge point is formed properly in the ventral neural tube
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• at E9.5, about 42% of embryos exhibit a cranial neural tube closure defect (NTD) in the form of exencephaly
• exencephalic embryos show failed bending of the neural folds at the dorsolateral hinge point
|
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• in the 58% of embryos that are not exencephalic, the telencephalic roof plate is malformed
• roof plate strucutures including the cortical hem, dorsal hippocampal primordium, and the choroid plexus are either hypomorphic or missing
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digestive/alimentary system
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• cleft palate is first observed in E14.5 embryos
• is observed in 42.9% of embryos between E16.5-E18.5
• is observed in 28.1% of neonates
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cellular
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• E9.5 embryos have excessive apoptosis in the hindbrain region and in adjacent craniofacial tissues
• there is a 2-fold increase in apoptosis of the mesenchymal cells
• there is also a 2-fold increase in apoptosis of the neuorepithelial cells of the E9.5 rostral hindbrain, and a 3-fold increase in the caudal hindbrain
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