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Fig. 7. Model of DMP development in mutant backgrounds. Shh has multiple
roles in AV septation, depicted by schematic sagittal sections at E11.5.
(A) Shh produced by foregut endoderm (blue) signals to adjacent DM
(green) allowing for mesenchymal movement into the atria and subsequent
formation of the DMP. DM-derived endocardium (dark green) and splanchnic
mesoderm (red) are also added to the atria at this time. (B) Global
loss of Shh results in a failure of DMP development as well as
abnormal AV cushion shape, probably owing to OFT and right ventricle
shortening. (C) Loss of receptiveness for Hh signaling in the
myocardium, endocardium and mesenchyme derived from the endocardium
(TnT-Cre; Tie2-Cre; Smoflox/-) does not recapitulate the
Shh-null AVSD phenotype. (D) While Shh is maintained
in Mef2C-AHF-Cre; Smoflox/- mutants, lack of receptiveness
in DM leads to failure of these cells to develop into the DMP.