Skip to main content
. 2008 Jan;19(1):378–393. doi: 10.1091/mbc.E07-01-0008

Table 1.

Abl overexpression and Bcr-Abl misexpression cause embryonic lethality

Driver Transgene % embryonic lethalitya nb
e22-GAL4 p185 (17) 100 389
p185 (6a1) 78 343
p185-Y177F (14b) 80 255
p210 (31) 96 350
p210 (11a) 56 355
p210 (6) 64 348
P210 kinase dead (11a) 8 347
P210 kinase dead (15a) 2 361
Wild-type Abl (UA3) 68 698
Kinase-dead Abl (UL6) 8 366
arm-GAL4:VP16 p185 (17) 100 240
p185 (6a1) 100 319
P185-Y177F (14b) 100 257
p210 (11a) 96 309
p210 (11) 100 298
P210 kinase dead (15a) 8 333
Wild-type Abl (UA22) 82 319
Wild-type Abl (UA3) 100 328
Kinase-dead Abl (UL1) 4 174
en-GAL4 p185 (17) 12 242
p185 (6a1) 12 238
p210 (31) 12 464
Wild-type Abl (UA22) 4 167

a Corrected for fraction of embryos of correct genotype. Both e22-GAL4 and arm-GAL4:VP16 are heterozygous, so only 50% of the embryos receive the driver and thus could be affected. Some of the transgenes were also maintained as balanced stocks and thus are also heterozygous.

b Number of embryos scored.