Table 1.
Genotype | Phenotype | |
---|---|---|
Hoxc-8 transgene | ||
TA/++/+ | Viable | |
TA/TA+/+ | Viable | |
+/+TR/+ | Viable | |
+/+TR/TR* | Viable | |
TA/+TR/+*† | Open eyes at birth, viable | |
TA/+TR/TR† | Open eyes, neonatal lethal | |
TA/TATR/+† | Open eyes, neonatal lethal | |
TA/TATR/TR‡ | Open eyes, perinatal lethal | |
Hoxd-4 transgene | ||
+/+TR/+ | Viable | |
TA/+TR/+‡ | Open eyes, neonatal lethal | |
Isl-1 transgene | ||
+/+TR/+ | Viable | |
TA/+TR/+† | Posterior growth defect |
All transgenes were on the FVB inbred background. In all TA mice used, VP16 expression is controlled by the Hoxc-8 promoter (14). The generation of TR strains was reported elsewhere (15). Results were obtained as follows: ∗, with two independent TA strains:
, with two independent TR stains; or
, with one combination of TA and TR strain.