In addition to the amino acid replacement, the progenitor P{GSV1}EndoGIGScE6 insertion has been precisely excised from the mutant chromosome.
Amino acid replacement: ?82term.
C16258426T
Q82term | EndoGI-PA; Q82term | EndoGI-PB; Q82term | EndoGI-PC
?82term
In addition to the amino acid replacement, the progenitor P{GSV1}EndoGIGScE6 insertion has been precisely excised from the mutant chromosome.
Homozygous clones in the wing disc grow as well as their wild-type twin spot clones.
Homozygous animals do not eclose at the expected frequency (there is a 70% reduction compared to heterozygotes).
EndoGIcwk/Df(2L)RA5 larvae grow more slowly than controls. Adult escapers are small and strikingly uncoordinated. They show a number of phenotypes, including tremors, crossed legs, an inability to right themselves and held-out wings.
Mutant embryos have motor axon defects. The most frequent and dramatic effect is on the intersegmental nerve b (ISNb) which fails to defasciculate from the ISN in 53% of hemisegments. The entire ISN nerve occasionally fails to exist the central nervous system. Defects in segmental nerve c (SNc) are seen in 39% of hemisegments and defects in the SNa are seen in 42% of hemisegments.
Only 19% of mutant females can fly.
EndoGIcwk has abnormal neuroanatomy | embryonic stage phenotype, suppressible | partially by Abl1/Abl[+]
EndoGIcwk has larval intersegmental nerve branch ISNb of A1-7 phenotype, suppressible | partially by Abl1/Abl[+]
EndoGIcwk is partially rescued by EndoGIUAS.cOa/Scer\GAL4elav.PLu
Expression of EndoGIScer\UAS.cOa under the control of Scer\GAL4elav.PLu significantly improves the coordination of EndoGIcwk animals; 73% of females tested can fly. In addition, the motor axon defects seen in EndoGIcwk embryos are also partially rescued.