Figure 6.

Tbx1-GFP can partially rescue endogenous Tbx1Cre/-loss-of-function. Histological transverse sections through the heart at E14.5. (A)Tbx1Cre/- mice are functionally null and have PTA and VSD. Tbx1Cre/+;Tbx1-GFPflox/+ mutants are viable with normal heart histology. (B)Tbx1Cre/-;Tbx1-GFPflox/+ mutants exhibit complete rescue of outflow tract septation although half of the embryos have double outlet right ventricle (DORV). (C)Tbx1Cre/-;Tbx1-GFPflox/flox mutants all have ventricular septal defect (VSD), primarily with persistant truncus arteriosus (PTA) and one example of DORV.

Freyer et al. BMC Developmental Biology 2013 13:33   doi:10.1186/1471-213X-13-33
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