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Fig. 1. Nkx2.5^Cre/+; Shh^flox/- specifically ablates pharyngeal endodermal SHH and results in a failure of OFT septation. (A) Shh is detected by in situ hybridization in the pharyngeal endoderm (arrowheads) at E10.5. (B) Nkx2.5^Cre expression, as detected by R26R, demonstrates overlap with Shh expression in the pharyngeal endoderm alone (arrowheads). (C,D) Conditional ablation of Shh in E10.5 Nkx2.5^Cre/+; Shh^flox/- embryos results in the specific loss of pharyngeal endodermal Shh (arrow, C versus D), but not of notochord and floorplate Shh expression, as expected (arrowheads, C,D). (E-F') Ptch1^lacZ expression at E10.5 demonstrates a specific loss of Hh activity in the pharyngeal endoderm and overlying mesoderm and mesenchyme (arrows, F,F') while maintaining other domains of expression, such as in the floorplate of the neural tube (arrowheads, E-F'). (G-H') Wild-type and Nkx2.5^Cre/+; Shh^flox/- E18.5 ink injections (G,H) demonstrate a single OFT vessel in mutants (arrow in H), whereas section analysis (G',H') reveals a complete atrioventricular canal defect (arrows in H'). In all panels, arrows and arrowheads mark abnormal and normal findings, respectively, in mutants as compared with control embryos. B; brachiocephalic artery; LCC, left common carotid; LSub, left subclavian; OFT, outflow tract; RCC, right common carotid; RSub, right subclavian.

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