Table 1.
Crosses of transactivator (TA) to transresponder (TR) strain | Phenotype | |
---|---|---|
TA-9 | TR-Isl-1.5 | viable: short, kinked, short and kinked tail |
TA-9 | TR-Isl-1.81 | viable: short tail |
TA-239 | TR-Isl-1.16 | lethal, no tail |
TA-239 | TR-Isl-1.50 | viable and lethal: short to absent tail |
TA-239 | TR-Isl-1.73 | normal |
TA-239 | TR-Isl-1.81 | viable: short tail |
TA-239 | TR-Hoxc-8 | tail normal, rib cartilage defect (Ref. 22) |
TA-239 | TR-Hoxd-4 | tail normal, rib cartilage defect (Ref. 22) |
Isl-1 transgenic mice were generated by crossing mice containing a transactivator (TA) transgene and a transresponder (TR) transgene, respectively. The TA strains express the VP16 transactivator protein in the caudal region of developing embryos (25). The relative transactivation capacity of the two independent TA lines is 1.69 and 5.7, respectively (26); both TA lines produced comparable phenotypes. Phenotypes of Hoxc-8 and Hoxd-4 transgenic animals were reported previously (22). Here, five independent Isl-1 TR strains were used, four produced caudal growth defects. The pictures in Fig. 1 E,F show animals generated with the Isl-1.16 TR line, all other studies reported here used the Isl-1.50 TR strain.