Fig. 5. Whole-mount in situ with markers of outflow tract myocardium. (A,B) 10.5 dpc wild-type (A) and Pitx2 c^-/- (B) embryos hybridized with semaphorin 3c probe. (C,D) 11.5 dpc wild-type (C) and Pitx2 c^-/- (D) embryos hybridized with semaphorin 3c probe showing expression in outflow tract myocardium (arrows). (E,F) 12.5 dpc wild-type (E) and Pitx2 c^-/- (F) embryos hybridized with semaphorin 3c probe showing that expression of semaphorin 3c is reduced in the mutant (n=3) (arrows). (G,H) Whole-mount views of 12.5 dpc wild-type (G) and Pitx2 abc^creneo;abc^null (H) null mutant embryos. Pitx2 abc^creneo;abc^null embryos demonstrate embryonic rotation, anterior body wall closure defects and eye anomalies typical of Pitx2 null embryos. (I,J) 12.5 dpc wild-type (I) and Pitx2 abc^creneo;abc^null (J) embryos hybridized with cre probe showing expression in outflow tract and right ventricular myocardium (arrows).

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