Fig. 1. Conditional loss and gain of β-catenin function causes mesoderm and segmentation phenotypes. (A-C) Wnt/β-catenin (BATlacZ) reporter activity in E9 wild-type (A), T-Cre;Ctnnb1^flLOF/ (B) and T-Cre;Ctnnb1^flGOF/+ (C) embryos. β-galactosidase (β-gal) activity was reduced posteriorly in the truncated T-Cre;Ctnnb1^flLOF/ mutants, and highly upregulated in the grossly enlarged PSM of the T-Cre;Ctnnb1^flGOF/+ embryo. In addition to the somite defects, kinked neural tubes, and an enlarged alantois were observed in the GOF mutants, whereas enlarged pericardia, and heart-looping defects were found in both LOF and GOF mutants. Bars, segment borders; curved line, the extent of the PSM. (D-Q) BATlacZ expression in 5 ss wild-type (D-F), T-Cre;Ctnnb1^flLOF/ (I-K), and T-Cre;Ctnnb1^flGOF/+ (N,O) embryos. (E,J) Cross-sections through the PS and PSM (level indicated by dotted lines in F and K) illustrate that the remaining β-gal activity in the T-Cre;Ctnnb1^flLOF/ PS (I) was found only in the ectoderm and not in the mesoderm (arrow in J). (G,H,L,M,P,Q) Hematoxylin and Eosin stained sections of E8.5 wild-type (G,H), T-Cre;Ctnnb1^flLOF/ (L,M), and T-Cre;Ctnnb1^flGOF/+ (P,Q) embryos. High-power magnifications illustrated in H, M and Q are taken from boxed regions in G, L and P. The asterisk in P indicates the kinked neural tube. All embryo images are lateral views, with the exception of F, K, and O, which offer a ventral-posterior perspective. S0, forming somite; SI, first somite; ps, primitive streak; psm, presomitic mesoderm; nt, neural tube. Scale bars: 100 µm.