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. Author manuscript; available in PMC: 2007 Mar 19.
Published in final edited form as: Dev Dyn. 2007 Mar;236(3):671–683. doi: 10.1002/dvdy.21059

Fig. 8.

Fig. 8

G1 causes a lack normal rotation of the outflow tract (OFT) and a ventricular septal defect (VSD). Confocal analysis of hearts from embryos injected with adenovirus into the anterior heart field (AHF; branchial arch 2) at stage 20 and incubated until Hamburger and Ham-ilton stage (HH) 29. A: Control, LacZ-infected hearts display the pulmonary artery at a depth of 50 μm and the aorta positioned dorsally at a depth of 200 μm, due to the normal rotation of the pulmonary trunk. B–D: Different G1-infected embryos where the aortic and pulmonary arteries are within the same plane of section (175 μm depth). E,F: A pronounced ventricular septal defect is apparent in the G1-infected hearts (arrow in F) when compared with the intact interventricular septum of the control heart in E. PA, pulmonary artery; Ao, aorta; LA, left atrium; RA, right atrium; LV, left ventricle; A3, aortic arch artery 3; A6, aortic arch artery 6. Scale bar = 400 μm in A (applies to B–F).