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Fig. 2. Cardiac OFT defects in newborn Alk2/Wnt1-Cre mice. (A) Functional domains of the ALK2 protein and schematic presentation of the Alk2 locus, the floxed and knockout alleles. Cre-mediated recombination results in excision of exon 7 flanked by the loxP sites (Alk2^Flox allele; red arrowheads), which encodes the Smad interacting domain (the L45 loop) and a crucial part of the kinase domain. This recombination results in generation of a null allele (Alk2^KO), which is biochemically inactive (Dudas et al., 2004). Blue arrows depict primers used to identify the Alk2^Flox allele. Intron 6 and intron 7 specific primers (green and blue arrows, respectively) were used to identify the Alk2^KO allele. (B) Homozygous floxed Alk2 (Alk2^Flox/Flox) mice were bred with Wnt1-Cre mice that are heterozygous for the Alk2 knockout allele (Alk2^KO) to produce a NC-specific deletion of exon 7. (C) Normal anatomy is seen in the control heart with the aorta (Ao) arising to the left and dorsal to the main pulmonary artery (PA) (left). The Alk2 mutant displays an abnormal single OFT, persistent truncus arteriosus (TA) (right). Moreover, the right ventricle (RV) of the mutant heart (right) is significantly larger than that of the control (left), and the brachiocephalic artery (BC) is short in the Alk2 mutant (C, frontal view and D, lateral view). Atria have been removed to facilitate better visualization of the OFTs. LV, left ventricle; RV, right ventricle. RS, right subclavian artery; RC, right common carotid artery; LC, left subclavian artery. (E) Hematoxylin and Eosin staining shows that the thymus is unaffected in Alk2/Wnt1-Cre mutants (right) compared with controls at E14.5 (left). Scale bar: 100 µm.

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