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Table 4.

Pharyngeal arch artery (PAA) development in Fgf8/hoxa3-IRESCre mutants: assessed by India ink injection at E10.5

GenotypeNormalAplastic PAAs 4 and 6Aplastic PAA 4 bilateralHypoplasia PAA 4 bilateralHypo/aplastic PAA 4, LHypo/aplastic PAA 4, R
AP/+ (n=19) 19 (100%) 
AP/+; hoxa3-ICre (n=19) 19 (100%) 
AP/N (n=17) 11 (65%) 1 (6%)* 6 (34%) 
AP/N; hoxa3-ICre (n=18) 5 (24%) 6 (28%) 4 (20%)§ 3 (15%) 3 (15%)** 
GenotypeNormalAplastic PAAs 4 and 6Aplastic PAA 4 bilateralHypoplasia PAA 4 bilateralHypo/aplastic PAA 4, LHypo/aplastic PAA 4, R
AP/+ (n=19) 19 (100%) 
AP/+; hoxa3-ICre (n=19) 19 (100%) 
AP/N (n=17) 11 (65%) 1 (6%)* 6 (34%) 
AP/N; hoxa3-ICre (n=18) 5 (24%) 6 (28%) 4 (20%)§ 3 (15%) 3 (15%)** 

These results show that there is no increase in incidence or severity of fourth PAA defects when FGF8 is ablated from the endodermal domain in addition to the ectodermal domain, and support our conclusion that the ectoderm supplies the required signal for fourth PAA vasculogenesis.

*

Severe hypoplasia

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 right PAA 4 aplasia

Three embryos had bilateral PAA 4 and 6 aplasia; two had PAA 4 and 6 aplasia on the right with PAA 4 aplasia on the left

§

Two embryos had severe hypoplasia of the entire left sided system

One embryo was aplastic

**

All three embryos were aplastic

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