Fig. 5. Loss of Fgf8 specifically disrupts the Isl1/Mef2c pathway in the AHF. In situ hybridized embryos; genotypes listed at the top, riboprobe and somite stage at the left. (A) Mef2c in 10ss embryos; right lateral view, red arrowheads indicate decreased signal in the OFT and AHF/SM of mutants. (A') Dorsal views; the ring of staining around the nascent OFT is markedly less intense in the mutants (red arrowheads). (B,B') Wnt11 at 20-21ss; close up of right side of the heart. Note the undetectable signal in the OFT myocardium of severe mutants (red arrowheads), and decreased levels in the mild variants (B'); expression is intact in Fgf8^C/-;Mef2cAHFCre mutants (black arrowhead). (C-C'') Pitx2 at 15ss; right lateral views in C, transverse sections in C',C''. Upper panels are at the level of the OFT, lower panels at level of the atrium/sinus venosus. (D,D') Tbx1 expression in transverse-sectioned 9-10ss embryos appears normal in the endoderm and SM/AHF. (E,E') Fgf10 in transverse-sectioned 8ss embryos. Expression is intact (black arowheads) except in mutant proximal OFT myocardium (red arrowheads).