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Fig. 3. Abnormal atrioventricular morphology in Tbx2^tm1Pa/Tbx2^tm1Pa mutants (–/–), 9.5-10.5 dpc. (A-C) Left views of a wild-type embryo (A, +/+) and two homozygous mutants (B,C) with abnormal atrioventricular (AV) morphology at 9.5 dpc. (D-F) Enlarged images highlight the AV canal that in wild type is distinguishable by the presence of a morphological constriction, indicated with the yellow arrowhead (D). Homozygous mutants frequently lack this AV constriction (E) or exhibit an enlarged or dilated ventricle (F). Left views of a (G) normal heterozygous embryo and a (H) homozygous mutant at 10.5 dpc. White lines in G indicate the planes of section for histology in J-O. The homozygous embryo in H shows signs of circulatory distress. (I) Closer inspection of another affected homozygous mutant shows a lack of constriction at the AV canal (red arrowheads). (J-L) Transverse histology at the outflow tract (OFT) of wild-type and homozygous mutant embryos at 10.5 dpc. Homozygous mutants that appear morphologically normal by external criteria show normal OFT endocardial cushion development (K). Distressed homozygous mutants have small endocardial cushions and the OFT appears to be shortened (L). (M-O) Transverse histology at the AV canal of the same embryos shown in J-L. Some homozygous mutants have normal endocardial cushion formation (N). Distressed homozygous mutants show compromised cushion formation (O). v, ventricle; a, atrium; oft, outflow tract; rv, right ventricle; ec, endocardial cushion.

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