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. 2018 Jan 1;145(1):dev159905. doi: 10.1242/dev.159905

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© 2018. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 5. — Cardiac-specific gain/loss of Wnt function modulates vascular fate in vivo. (A-C) Whole-mount confocal images of TCF/Lef:H2B-GFP;Cdh5^Cre;Rosa^tdTom mouse embryos at E8.0 (A) and E8.5 (B) and isolated heart at E11.5 (C). Arrowheads (A-C) indicate ECs; arrows indicate (A) an EC that is faintly positive for TCF/Lef:H2B-GFP or (B,C) TCF/Lef:H2B-GFP⁺ cells. (D,E) The β-catenin^LOF strain was crossed with Flk1-GFP;Nkx2.5^Cre;Rosa^tdTom mice to generate embryos with heterozygous and homozygous ablation of β-catenin. z-stack projections are compared (D) and sagittal and coronal sections are shown (E). (F) The percentage of NkxECs was quantified for the left and right ventricles of β-catenin^LOF versus heterozygous littermates. Error bars represent s.d. between five biological replicates. *P<0.05. (G,H) β-catenin^GOF males were crossed with Flk1-GFP;Nkx2.5^Cre;Rosa^tdTom females to generate embryos with constitutively active Wnt signaling in the heart. β-catenin^GOF embryos versus control littermates are shown at E9.0 and E9.5 (G) and total EC number and percentage NkxECs were measured for ventricles, atria and outflow tract of β-catenin^GOF versus control littermate hearts between E8.5 and E9.5 (H). Scale bars: A-E,G, 100 µm.