aPKCSG58/aPKC[+] is a suppressor of visible phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF
aPKCSG58/aPKC[+] is a suppressor of abnormal neuroanatomy | adult stage phenotype of DCTN1-p150Δ.UAS, Scer\GAL4shot-OK307
aPKCSG58/aPKC[+] is a suppressor of abnormal neurophysiology | adult stage phenotype of DCTN1-p150Δ.UAS, Scer\GAL4shot-OK307
aPKCSG58/aPKC[+] is a suppressor of eye phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF
aPKCSG58/aPKC[+] is a suppressor of giant fiber neuron phenotype of DCTN1-p150Δ.UAS, Scer\GAL4shot-OK307
aPKCSG58 dominantly suppresses the eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF.
aPKCSG58/+ mildly suppresses the swollen tip phenotype of giant fiber axons expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307, but the lack of a terminal bend phenotype is not rescued.
Heterozygosity for aPKCSG58 partially suppresses the giant fiber system electrophysiological defects in animals expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307; all preparations respond to stimulation, there is a slight reduction in the long response latency and a corresponding increase in following to repetitive stimuli.
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.