Analysis Tools
mortality/aging
|
• homozygous null mice died at approximately 10.5 dpc, probably due to heart and circulatory system failure
|
cardiovascular system
|
• at 9.5 dpc, homozygous null embryos showed reduced trabeculation of the ventricular walls
|
|
• homozygous null embryos exhibited an abnormal constriction between the atria and the ventricle, and presented a looping defect indicating arrested cardiac development
|
|
• homozygous null embryos displayed an enlarged pericardial sac
|
hemorrhage
(
J:42030
)
|
• sudden hemorrhage occurred prior to cardiac cessation and death shortly after 10.5 dpc, but never before 9.75 dpc
|
embryo
|
• mutant branchial arches appeared highly pyknotic and hypoplastic
|
|
• homozygous null embryos displayed severe loss or ablation of paraxial mesoderm, manifested as reduced cellularity and tissue failure in the paraxial mesenchyme
|
|
• mutant forelimb buds appeared smaller relative to wild-type
|
|
• hindlimb buds were rarely observed in mutant embryos
|
|
• at 10.5 dpc, the mutant mesonephric ducts and tubules appeared smaller and hypocellular relative to wild-type
|
|
• homozygous null embryos had decreased numbers of somite pairs after the 32 somite (~10.25 dpc) stage
|
|
• the mutant amnion was filled with fluid and attached to the yolk sac at multiple sites
|
pale placenta
(
J:42030
)
|
• homozygous null embryos displayed a pale placenta relative to wild-type
|
pale yolk sac
(
J:42030
)
growth/size/body
liver/biliary system
|
• at 10.5 dpc, the mutant liver primordium appeared highly pyknotic and hypoplastic relative to wild-type
|
muscle
|
• at 9.5 dpc, homozygous null embryos showed reduced trabeculation of the ventricular walls
|
|
• at 10.5 dpc, the mutant myotome was either highly hypoplastic or absent
|
|
• at 10.5 dpc, the mutant myotome may be absent
|
nervous system
| N |
• homozygous null embryos displayed marked hypocellularity ventral to the neural tube from the cephalic flexure in the head and extending posteriorly to the level of hindlimb bud
|
|
• growth of the telencephalic vesicles was consistently reduced
|
|
• most homozygous null embryos displayed malformation of the inferior region of the diencephalon near the cephalic flexure
|
|
• at 9.5-9.75, mutants showed defective formation of the cranial accessory neuron
|
|
• at 9.5-9.75, mutant embryos consistently exhibited defective formation of the superior regions of the glossopharyngeal ganglion
|
|
• the mutant trigeminal ganglion complex and the facio-acoustic complex were hypoplastic
|
|
• at 9.5-9.75, mutants showed defective formation of the superior vagal ganglion
|
|
• in contrast to wild-type embryos, mutant embryos failed to display spinal neuron development at 10.0-10.25 dpc
|
craniofacial
|
• mutant branchial arches appeared highly pyknotic and hypoplastic
|
limbs/digits/tail
|
• mutant forelimb buds appeared smaller relative to wild-type
|
|
• hindlimb buds were rarely observed in mutant embryos
|
skeleton
|
• at 10.5 dpc, mutant sclerotomal cells became hardly discernible relative to wild-type
|
