Fig. 6. Components of the Notch pathway participate in a Wnt3a-dependent pathway that controls laterality and somitogenesis. (A-D) Whole-mount in situ hybridization analysis of Dll1 expression in E8 wild-type (A,C) and Wnt3a^-/- (B,D) embryos. Dll1 expression in the psm surrounds the wild-type node (C), but only abuts the posteriormost node in a Wnt3a^-/- embryo (D). The lines in A and B, and ovals in C and D, indicate the location of the node. (E-H) Histological sections of wild-type neonatal heart (E), and three examples of cardiac laterality defects in compound Wnt3a^vt; Dll1 mutants, including PTA (arrow, F), TGA (G) and VSD (arrow, H). (I,J) Axin2 expression in the streak, psm and in an anterior stripe (presomite 0) in wild-type one-somite embryos (I), was downregulated in Wnt3a^-/- mutants and no psm stripes were observed (J). (K,L) Two color whole-mount in situ hybridization on four-somite stage embryos, illustrating (K) cycling Lfng (purple) and Nodal expression (orange) in the wild-type left LPM. Dynamic Lfng expression was not observed in the absence of Wnt3a, as only a single psm stripe was observed in the Wnt3a mutants (L). Nodal was not expressed in the mutant LPM at these stages.