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. Author manuscript; available in PMC: 2014 Apr 7.
Published in final edited form as: FASEB J. 2003 May 8;17(10):1349–1351. doi: 10.1096/fj.02-0856fje

Table 1.

Caudal growth defects are Isl-1 transgene specific

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.