EG28EG28/EG28[+] is an enhancer of abnormal neurophysiology | adult stage | dominant phenotype of DCTN1-p150Gl-1
EG28EG28/EG28[+] is an enhancer of visible phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF
EG28EG28/EG28[+] is a non-enhancer of abnormal neuroanatomy | adult stage phenotype of DCTN1-p150Δ.UAS, Scer\GAL4shot-OK307
DCTN1-p150Δ.UAS, EG28EG28/EG28[+], Scer\GAL4shot-OK307 has abnormal neuroanatomy | adult stage phenotype
DCTN1-p150Gl-1, EG28EG28/EG28[+] has abnormal neuroanatomy | dominant | adult stage phenotype
EG28EG28/EG28[+] is an enhancer of eye phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF
EG28EG28/EG28[+] is a non-enhancer of giant fiber neuron phenotype of DCTN1-p150Δ.UAS, Scer\GAL4shot-OK307
DCTN1-p150Δ.UAS, EG28EG28/EG28[+], Scer\GAL4shot-OK307 has giant fiber neuron phenotype
DCTN1-p150Gl-1, EG28EG28/EG28[+] has giant fiber neuron phenotype
EG28EG28 dominantly enhances the eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF.
20% of giant fiber axons fail to exit the brain in adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 in a EG28EG28/+ background.
Only 3% of giant fiber axons in Gl1/+ ; EG28EG28/+ double heterozygotes lack the characteristic terminal bend, but the axons often show ectopic branching.
The electrophysiological defects seen in the giant fiber system of Gl1/+ adults are enhanced if they are also heterozygous for EG28EG28; 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.