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Fig. 5. AHF ablation of Hh signaling results in a single OFT due to septation failure, but not in a shortened OFT. (A,B) Ink injections of wild type (A) and AHF-Cre; Smo^flox/- (B) at E18.5 reveals a single OFT in the mutants. (C-F) ß-galactosidase staining in AHF-Cre; Smo^flox/- mutants that are also transgenic for Tie2-lacZ reveals that the OFT is not significantly shortened (D,D') and that cushions form (D',F) similar to control (C,C',E) embryos (bar length is identical in C,D). Arrowheads point to cushions compressing the endothelial channel in C',D'. (E,F) Section analysis of E10.5 AHF-Cre; Smo^flox/- mutants also transgenic for the Cre reporter R26R (F) reveals that CNCCs populate the OFT cushions in relatively normal numbers compared to controls (E). (G-H') Although the cushions are well-formed at E12.5 (H,H', arrows), septation does not complete in AHF-Cre; Smo^flox/- mutants, resulting in a single OFT channel (H,H') compared with controls (G,G'). (I,J) Ptch1^lacZ expression in AHF-Cre; Smo^flox/- mutants reveals a specific loss of expression within the AHF, including in the expression entering the OFT (J versus I, arrow). In all panels, arrows and arrowheads mark abnormal and normal findings, respectively, in mutants as compared with control embryos. Ao, aorta; Pa, pulmonary artery; OFT, outflow tract; RA, right atrium; LV, left ventricle.

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