Analysis Tools
mortality/aging
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• one third of homozygous embryos survive to birth but then die within the first four days after birth
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• development is normal to E9.5
• about two thirds of homozygotes die between E10 and E12
• remaining embryos normal
• heart is not beating in about 20% of E10.5 embryos
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embryo
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• about 50% were smaller than littermate controls
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• floor plate of neural tube is absent in mice destined to die by E11.5
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• in 50% of mice destined to die by E11.5
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• primary vascular plexus less complex and with less branching than controls
• some dilation of blood vessels observed
• confirmed in mice carrying the Tg(TIE2-lacZ)182Sato/0 transgene
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• fewer fetal blood vessels or absence of such vessels
• allantoic and fetal placental blood sinuses frequently dilated and filled with fetal red blood cells
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• less vascularized than controls
• fewer fetal blood vessels penetrate the layer and sponge-like vascular network missing
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• labyrinthine zone of placenta dramatically reduced in thickness
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pale yolk sac
(
J:77682
)
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• 5 of 41 viable homozygous embryos show abnormally loose allantois-chorion connections at E10.5
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cardiovascular system
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• endothelial cells of blood vessels are hyperproliferative
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• capillaries fail to penetrate the neuroepithelium from the perineural plexus in embryos that fail to survive to birth
• mice that survive have grossly normal capillaries at E11.5 but hemorrhaging occurs
• capillaries are present as aggregates forming complex structures
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• fewer fetal blood vessels or absence of such vessels
• allantoic and fetal placental blood sinuses frequently dilated and filled with fetal red blood cells
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• less vascularized than controls
• fewer fetal blood vessels penetrate the layer and sponge-like vascular network missing
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• failure of capillary vesseles to penetrate very far into the neuroepithelium
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• branching defect but original vasculogenesis is normal
• confirmed in mice carrying the Tg(TIE2-lacZ)182Sato/0 transgene
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• primary vascular plexus less complex and with less branching than controls
• some dilation of blood vessels observed
• confirmed in mice carrying the Tg(TIE2-lacZ)182Sato/0 transgene
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• in embryos destined to die by E11.5
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• ventricles less vascularized
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• pericardial cavity often dilated
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• in embryos surviving to birth hemorrhage first appears at E12.5 in ganglionic eminence
• spreads to diencephalons, then cortex and mantle layers of hindbrain
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nervous system
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• in embryos surviving to birth hemorrhage first appears at E12.5 in ganglionic eminence
• spreads to diencephalons, then cortex and mantle layers of hindbrain
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• radial glial cells in neuroepithelium become poorly aligned between E10.5 and E12.5
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• floor plate of neural tube is absent in mice destined to die by E11.5
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hydrocephaly
(
J:77682
)
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• seen in mice that survive to birth
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• in mice surviving to birth, bilateral cavitation is found in subventricular areas surrounding all four ventricles by E11.5
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growth/size/body
cleft palate
(
J:77682
)
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• about 10% of embryos that survive past E11.5 display cleft palate
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• about 50% were smaller than littermate controls
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craniofacial
cleft palate
(
J:77682
)
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• about 10% of embryos that survive past E11.5 display cleft palate
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digestive/alimentary system
cleft palate
(
J:77682
)
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• about 10% of embryos that survive past E11.5 display cleft palate
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homeostasis/metabolism
cellular
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• radial glial cells in neuroepithelium become poorly aligned between E10.5 and E12.5
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• discontinuous expression of fibronectin and laminin at E14.5 indicates abnormalities in the basement membranes of brain capillaries
• no failure of assembly
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