Compound action potentials can be evoked by sound in the antennal nerve of mutant flies, but the sound particle velocities required to elicit the response is increased compared to wild type. The displacement response of the antenna over a range of sound particle velocities is linearised, indicating loss of mechanical amplification.
In whole-cell voltage-clamp recording of dissociated ommatidia from Arr25 flies, 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.
The response to a brief flash in dissociated ommatidia from Arr25 flies shows a prolonged decay lasting several seconds, the tail of which can be fitted with a single exponential of approximately 1400ms. This slow deactivation is due to single photons exciting trains of quantum bumps, with refractory periods ranging from 50 to approximately 150ms. In Ca[2+]-free conditions, responses in Arr25 flies are prolonged compared to wildtype, with an intermediate time course observed for Arr25 heterozygotes.
In regular cyclic illuminating conditions, 7 day old mutant flies have smaller rhabdomeres than normal and have large intracellular vacuoles in the photoreceptors. The shape of the rhabdomere is normal in these flies.
The termination speed of photoresponses in Arr25 flies is slower than for wild-type flies.
In an electroretinogram of dark-reared, newly eclosed Arr25 mutant flies, photoreceptor receptor cells rapidly depolarise and remain depolarised during the light stimulus, as in wild-type, but once the light stimulus is terminated the photoreceptor cells re-polarise very slowly, taking about four times longer to terminate the response.
Eyes from Arr25 mutant flies exposed to 5 days of constant light show severe retinal degeneration. Large intracellular holes develop and the ommatidial organization is completely lost.
Eyes from Arr25 mutant flies exposed to a 12-hour light/dark cycle from 30 days show severe and almost complete retinal degeneration, with all except the R7 rhabdomere completely missing.
Arr25 mutants display retinal axon termination responses that are comparably slow after both long (3-seconds) and short (0.2-seconds), compared to wild-type.
Light-induced currents of Arr25 photoreceptor cells are almost identical to those of wild-type flies.
4-day-old Arr25 mutants show slightly smaller and abnormally shaped rhabdomeres, relative to wild type.
The reduction in electroretinogram (ERG) amplitude seen in flies exposed to constant light is greatly suppressed by Arr25 or Arr25/Arr23KQ. However, retinal degeneration and rate of loss of the deep pseudopupil in Arr25/Arr23KQ flies exposed to constant light is the same as that seen in wild-type flies exposed to constant light.
The termination of the electroretinogram (ERG) response to light is slower in Arr25 flies than in wild-type flies. Preexposure to light has very little impact on the rate of termination of the ERG in Arr25 flies, in contrast to wild-type flies where preexposure to light increases the speed of termination of the ERG response. The termination of the electroretinogram (ERG) response to light is slower in Arr25 flies carrying Arr23KQ than in wild-type flies. Preexposure to white light for 10 minutes results in an increase in the rate of termination of the ERG (as occurs in wild-type flies), but the rate of termination is much slower than in wild-type flies.
After 6 days of exposure to continuous room light, null Arr2 mutants exhibit a light dependant retinal degeneration phenotype. The photoreceptor rhabdomeres are present, but numerous large intra cellular vacuoles completely disrupt ommatidial organisation.
Flies show complete retinal degeneration based on deep pseudopupil analysis after 3-4 days of light exposure. No significant degeneration is seen in the dark, even after several weeks of exposure. Electroretinograms of mutant flies have marked defects in inactivation kinetics, with an increase in the time required to reach 85% inactivation.