Fig. 6.

Marker analysis in β-catenin loss-of-function and gain-of-function mutant embryos. (A–L) Analysis of markers for SHF and differentiated myocardium in 9.5-dpc embryos. Genotypes and markers are labeled. Pharyngeal mesenchyme is denoted by yellow arrowheads, and OFT is denoted by black arrowheads. OFT is outlined by a dotted line in G–I for clarity. (M) Model depicting the proposed role of canonical Wnt signaling in SHF. Based on loss- and gain-of-function experiments, canonical Wnt signaling promotes Bmp4 expression while concurrently acting to restrict Fgf10 in the SHF. The dotted line for Fgf10 repression indicates that this may be a minor function for Wnt signaling in the SHF because the data supporting this inhibitory function were observed only in the gain-of-function experiment. In the SHF-derived myocardium of the OFT, RV, and interventricular septum (IVS), canonical Wnt signaling regulates Bmp4 and promotes cell proliferation through regulation of Cyclin D. ba, branchial arch; RV, right ventricle; lv and LV, left ventricle; oc, otic capsule.