Figure 6.

Tbx1-GFP can partially rescue endogenous Tbx1^Cre/-loss-of-function. Histological transverse sections through the heart at E14.5. (A)Tbx1^Cre/- mice are functionally null and have PTA and VSD. Tbx1^Cre/+;Tbx1-GFP^flox/+ mutants are viable with normal heart histology. (B)Tbx1^Cre/-;Tbx1-GFP^flox/+ mutants exhibit complete rescue of outflow tract septation although half of the embryos have double outlet right ventricle (DORV). (C)Tbx1^Cre/-;Tbx1-GFP^flox/flox mutants all have ventricular septal defect (VSD), primarily with persistant truncus arteriosus (PTA) and one example of DORV.