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Table 2.

Pharyngeal arch artery (PAA) development in Fgf8/AP2α-Cre mutants: assessed by India ink injection at E10.5-11

Phenotype
GenotypeNormalAplastic PAAs 4 and 6Aplastic PAA 4 bilateralHypoplasia PAA 4 bilateralHypo/aplastic PAA 4, LHypo/aplastic PAA 4, R
AP/+ (n=41) 41 (100%) 
AP/+; AP2α-ICre (n=40) 40 (100%) 
AP/N (n=38) 24 (64%) 8 (21%)* 6 (16%) 
AP/N; AP2α-ICre (n=37) 2 (6%) 12 (33%) 12 (33%) 4 (12%) 4 (12%)§ 3 (8%) 
Phenotype
GenotypeNormalAplastic PAAs 4 and 6Aplastic PAA 4 bilateralHypoplasia PAA 4 bilateralHypo/aplastic PAA 4, LHypo/aplastic PAA 4, R
AP/+ (n=41) 41 (100%) 
AP/+; AP2α-ICre (n=40) 40 (100%) 
AP/N (n=38) 24 (64%) 8 (21%)* 6 (16%) 
AP/N; AP2α-ICre (n=37) 2 (6%) 12 (33%) 12 (33%) 4 (12%) 4 (12%)§ 3 (8%) 

These results indicate that the ectodermal domain of FGF8 is specifically required for correct formation of the fourth pharyngeal arch artery (PAA). Remodeling and recovery from these fourth PAA defects results in the array of vascular defects seen in Fgf8/Ap2α-Cre mutants at birth.

*

Four embryos had left PAA, four had hypoplasia and 4 had aplasia (nonpatent to ink)

Most of these are probably attributable to normal remodeling to the left-side dominant system, which we have observed to occur as early as E10.5 in the C57B16 background; one embryo had an aplastic right PAA 4

Eleven embryos had bilateral aplasia of PAAs 4 and 6; two embryos had aplasia of PAAs 4 and 6 on the right with PAA 4 aplasia on the left

§

Three embryos were aplastic

One aplastic

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