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. Author manuscript; available in PMC: 2011 Mar 16.
Published in final edited form as: Dev Cell. 2010 Mar 16;18(3):480–485. doi: 10.1016/j.devcel.2009.12.019

Table 1.

Outflow tract phenotypes in RA receptor mutant embryos.

A. Tamoxifen treatment of CAGG-Cre,RARα1−/−, RXRαflox/flox embryos
Injection
time
Mutants Litters CAT DORV Overriding
Aorta
Normal
E6.75–7.0 14 5 7 50% 3 21% 1 7% 3 21%
E7.5–8.0 17 7 5 29% 2 21% 2 12% 8 47%
E8.5 10 5 2 20% 2 20% 2 20% 4 40%
E9.0–9.5 17 8 0 0% 7 41% 4 21% 6 35%
E10.0–10.5 6 4 0 0% 0 0% 0 0% 6 100%
B. Tissue specific inactivation in Cre,RARα1−/−, RXRαflox/flox embryos
Cre line Mutants Litters CAT DORV Overriding
Aorta
Normal
Mesp1Cre 18 11 9 50% 3 17% 3 17% 3 17%
Myf5Cre 8 2 0 0% 0 0% 0 0% 8 100%
Mef2cCre 10 8 0 0% 0 0% 0 0% 10 100%
Tie2Cre 7 3 0 0% 0 0% 0 0% 7 100%
C. Rescue of septation in RARα1/RARβ mutants by reduction of TGFβ2 gene dosage
Genotype Mutants Litters CAT DORV Overriding
Aorta
Normal
RARα1−/−
RARβ−/−
* * * 100% 0 0% 0 0% 0 0%
RARα1−/−
RARβ−/−
TGFβ2−/+
9 7 4 44% 5 55% 0 0% 0 0%

A. CAGG-Cre,RARα1−/−, RXRαflox/flox embryos were isolated following a single i.p. tamoxifen injection at the indicated times, and analyzed for cardiovascular defects. B. Phenotypes were scored in RARα1−/−, RXRαflox/flox embryos carrying the indicated Cre genes. C. Phenotypes were scored in double receptor mutant embryos with or without heterozygosity of Tgfb2.

*

The complete penetrance of CAT in RARα1/RARβ embryos is based on some embryos from the current study plus many from earlier analyses, totaling over 100 embryos in all.