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Table 2.

Vascular defects in TIE-Δ4 angiomotin transgenic mice

Embryo TIE-Δ4 angiomotin (Southern blot) Phenotype
1   +   Cranial hemorrhage, cranial aneurysms  
2   +   Cranial hemorrhage, cranial aneurysms  
3   +   Cranial hemorrhage  
4   +   Cranial hemorrhage  
5   +   Cranial hemorrhage  
6   +   Cranial hemorrhage  
7   +   Cranial hemorrhage, not viable  
8   +   Cranial aneurysms  
9   +   Cranial aneurysms  
10   +   Cranial and cardiac malformation  
11   +   Cranial malformation  
12   +   Not viable  
13   +   Not viable  
14   +   No detectable phenotype  
15-100   Negative-litter mates   No detectable phenotype  
Embryo TIE-Δ4 angiomotin (Southern blot) Phenotype
1   +   Cranial hemorrhage, cranial aneurysms  
2   +   Cranial hemorrhage, cranial aneurysms  
3   +   Cranial hemorrhage  
4   +   Cranial hemorrhage  
5   +   Cranial hemorrhage  
6   +   Cranial hemorrhage  
7   +   Cranial hemorrhage, not viable  
8   +   Cranial aneurysms  
9   +   Cranial aneurysms  
10   +   Cranial and cardiac malformation  
11   +   Cranial malformation  
12   +   Not viable  
13   +   Not viable  
14   +   No detectable phenotype  
15-100   Negative-litter mates   No detectable phenotype  

No viable offspring could be generated from pronuclear injections with the TIE-Δ4 angiomotin construct. The vascular phenotype of embryos was therefore analyzed at E9.5. The DNA from the embryos was analyzed by Southern blot for transgene integration. 100 pronuclear injections resulted in 14 transgenic embryos. Note that each of these embryos reepresents an independent founder animal with a specific transgene integration site. The vascular phenotype of embryos was analyzed by whole-mount PECAM staining. The appearance of vascular defects was statistically significant (P<0.001) as analyzed by the Chi-square exact test.

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