mortality/aging
• homozygous null embryos died around E10 probably as a result of hemorrhage and edema in the heart and brain
|
cardiovascular system
• at E9, immunological and molecular analyses of the vascular system revealed a reduction in the extent and complexity of microvasculature in the head and spine regions, suggesting impaired angiogenesis and vascular remodeling
• angiogenic defects were consistent with a loss of function in the mesenchymal compartments of the head, spine, and heart
|
• by E9-E9.5, both anterior and posterior cardinal veins appeared either malformed or had collapsed
|
• by E9-E9.5, anterior cardinal vein appeared either malformed or collapsed
|
• by E9-E9.5, posterior cardinal vein appeared either malformed or collapsed
|
• at E9.5, some mutant embryos displayed a reduced trabeculation
|
• at E9.5, wild-type hearts displayed an enlarged common atrial chamber, whereas mutant hearts showed only a primitive atrial tube situated on the left
• the primitive atrial tube was connected to a small and primitive sinus venosus situated over the midline; as a result, the mutant pericardial-peritoneal cavity was empty
|
hemorrhage
(
J:54469
)
• at E9.5, homozygous null mice displayed hemorrhage in the frontonasal process and edematous cysts on the brain
• at E10-E10.5, mutant embryos displayed blood-filled brain vesicles and hemorrhagic hearts
|
embryo
N |
• placentas of homozygous mutant embryos developed normally
|
• at E10-E10.5, partially resorbed embryos contained less than 29 somites versus 30-35 somites typically observed in wild-type embryos
|
muscle
• at E9.5, some mutant embryos displayed a reduced trabeculation
|