Su(H)[+]/Su(H)EG37 is an enhancer of visible | dominant phenotype of DCTN1-p150Gl-1
Su(H)[+]/Su(H)EG37 is an enhancer of abnormal neurophysiology | adult stage | dominant phenotype of DCTN1-p150Gl-1
Su(H)[+]/Su(H)EG37 is an enhancer of visible phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF
Su(H)[+]/Su(H)EG37 is an enhancer of eye phenotype of DCTN1-p150Gl-1
Su(H)[+]/Su(H)EG37 is an enhancer of ommatidium phenotype of DCTN1-p150Gl-1
Su(H)[+]/Su(H)EG37 is an enhancer of rhabdomere phenotype of DCTN1-p150Gl-1
Su(H)[+]/Su(H)EG37 is an enhancer of eye phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF
Su(H)EG37 dominantly enhances the eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF.
Su(H)EG37 dominantly enhances the eye phenotype caused by Gl1, resulting in an increase in bristles and an increase in ommatidial fusion and disorganisation. There is increased disruption of accessory cells and rhabdomeres are often fused.
The electrophysiological defects seen in the giant fiber system of Gl1/+ adults are enhanced if they are also heterozygous for Su(H)EG37; 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.