EG56EG56/EG56[+] is an enhancer of abnormal neuroanatomy | adult stage | dominant phenotype of DCTN1-p150Gl-1
EG56EG56/EG56[+] is an enhancer of abnormal neurophysiology | adult stage | dominant phenotype of DCTN1-p150Gl-1
EG56EG56/EG56[+] is an enhancer of visible phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF
EG56EG56/EG56[+] is an enhancer of giant fiber neuron phenotype of DCTN1-p150Gl-1
EG56EG56/EG56[+] is an enhancer of eye phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF
EG56EG56 dominantly enhances the eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF.
The fraction of giant fiber axons that lack the characteristic terminal bend in Gl1/+ flies is increased if they are also heterozygous for EG56EG56.
The electrophysiological defects seen in the giant fiber system of Gl1/+ adults are enhanced if they are also heterozygous for EG56EG56; the response latencies are significantly increased and the double heterozygous flies show poor following.
It has not been determined whether the lethality of the chromosome is caused by the mutation that modifies the eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF, so it is possible that the recessive lethality of the chromosome is due to a second-site mutation.