Construct: Entire gene and upstream sequences of Rh3 are fused to 2.8kb ninaE promoter fragment containing 67 nucleotides of untranslated leader sequence.
Whole-cell voltage-clamp recordings of dissociated ommatidia from flies of the genotype ninaE17,Rh3Rh1+3 (in which the UV responsive Rh3 is driven in place of ninaE by this latter's promoter) show similar, albeit slightly slower, kinetics to responses from wildtype ommatidia. Quantum bumps are similar in waveform, but slightly larger than wildtype, and a similar dependence on Ca[2+] is seen.
Rh3Rh1+3 has abnormal neurophysiology phenotype, suppressible by ninaC5
Rh3Rh1+3 has abnormal neurophysiology phenotype, non-suppressible by ninaE17
Rh3Rh1+3 is a suppressor of abnormal neurophysiology phenotype of ninaC5
ninaE17/Rh3Rh1+3 is a non-suppressor of abnormal neurophysiology phenotype of Arr25
Rh3Rh1+3, ninaE17 has abnormal optomotor response phenotype
Rh3Rh1+3 has ommatidium phenotype, suppressible by ninaC5
Rh3Rh1+3 has ommatidium phenotype, non-suppressible by ninaE17
Rh3Rh1+3 is a suppressor of ommatidium phenotype of ninaC5
ninaE17/Rh3Rh1+3 is a non-suppressor of ommatidium phenotype of Arr25
In whole-cell voltage-clamp recording of dissociated ommatidia from Arr25 flies carrying Rh3Rh1+3 and mutant for ninaE17, the response to brief flashes of UV light inactivates normally but then fails to rapidly reach baseline leaving a secondary peak that decays over several seconds.
Flies expressing Rh3Rh1+3 in the ninaC5 mutant background show that the slowly decaying tail is rapidly suppressed by photoreconversion of metarhodopsin to rhodopsin.