Fig. 5
From: Msx1 haploinsufficiency modifies the Pax9-deficient cardiovascular phenotype
Deletion of Pax9 from the second heart field in C57Bl/6 congenic mice recapitulates the Pax9–/– cardiovascular phenotype. Embryos at E15.5 were imaged by MRI. A–C Pax9+/flox;Isl1Cre control embryos had normal development of the palate (A), thymus (B) and hind limb digit (white arrow; C). D–F Congenic C57Bl6/J Pax9–/flox;Isl1Cre embryos with a second heart field (SHF) conditional inactivation of Pax9 (B6-Pax9ΔSHF) display a normal palate (D), absent thymus (asterisk; E) and pre-axial digit duplication (red arrows; F). G–I Cardiovascular defects in B6-Pax9ΔSHF embryos. G Control embryos have normal heart and aortic arch artery development. H, I B6-Pax9ΔSHF embryos present with typical Pax9–/– cardiovascular defects such as double-outlet right ventricle (DORV) with interventricular communication (IVC), interrupted aortic arch type B (IAA-B), aberrant right subclavian artery (A-RSA), and absent common carotid arteries resulting in the internal and external carotid arteries (iLC, eLC, iRC, eRC) arising directly from the aorta and dorsal aorta respectively. AD, arterial duct; Ao, aorta; BC, brachiocephalic artery; LCC/RCC, left/right common carotid artery; LSA/RSA, left/right subclavian artery; LV/RV, left/right ventricle; P, palate; Th, thymus. Scale bars: 500 µm