Fig. 6
From: Msx1 haploinsufficiency modifies the Pax9-deficient cardiovascular phenotype
Deletion of Pax9 from the second heart field in neonates on an enriched CD1 background. A–C Pax9+/flox;Isl1Cre control neonates had normal hind limb digit (black arrow; A), palate (B) and arch artery (C) development. D–F Pax9–/– neonates from this cross displayed the typical Pax9–/– phenotype of pre-axial digit duplication (red arrows; D), cleft palate (black arrows; E) and cardiovascular defects such as interrupted aortic arch type B (IAA-B; F). G–I Only one neonate with Pax9 conditionally inactivated from the second heart field (Pax9ΔSHF) was recovered but showed a pre-axial digit duplication (red arrows; G), a normal palate (H) and IAA-B (I). J–L Pax9ΔSHF;Msx1+/– neonates displayed a pre-axial digit duplication (red arrows; J), a normal palate (K) and frequently mild arch artery defects such as cervical aortic arch (cAo) and abnormal external and internal left common carotid artery (eLC, iLC; L). Ao, aorta; AoA, aortic arch; CP, cleft palate; LCC/RCC, left/right common carotid artery; LSA/RSA, left/right subclavian artery. Scale bars: 1 mm