Amino acid replacement: Y20term.
T8648766R
Y20term | Arr2-PA
Y20term
Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
ommatidium, with Arr2S366A
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.
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.
Arr25 has abnormal neurophysiology phenotype, enhanceable by Camtates-2
Arr25 has abnormal neurophysiology phenotype, non-suppressible by ninaE17/Rh3Rh1+3
Arr25 is an enhancer of abnormal neurophysiology phenotype of Camtates-2
Arr25 is a suppressor of increased cell death phenotype of Arr11
Arr25 is a suppressor of abnormal neuroanatomy phenotype of trp9
Arr25 is a suppressor | partially of abnormal neuroanatomy phenotype of trp14
Arr25 is a suppressor | partially of abnormal neurophysiology | recessive phenotype of ninaEpp100
Arr25 is a suppressor | partially of increased cell death phenotype of ninaEpp100
Arr25/Gαq1 is a suppressor of increased cell death phenotype of ninaEpp100
Arr25 has eye photoreceptor cell phenotype, enhanceable by Camtates-2
Arr25 has retina phenotype, suppressible by su(rdgA)4040
Arr25 has ommatidium phenotype, suppressible by norpAEE5
Arr25 has ommatidium phenotype, non-suppressible by ninaE17/Rh3Rh1+3
Arr25 has eye phenotype, non-suppressible by BacA\p35GMR.PH
Arr25 has ommatidium phenotype, non-suppressible by BacA\p35GMR.PH
Arr25 has retina phenotype, non-suppressible by BacA\p35GMR.PH
Arr25 is an enhancer of eye photoreceptor cell phenotype of Camtates-2
Arr25 is a suppressor of eye photoreceptor cell phenotype of Arr11
Arr25 is a suppressor of rhabdomere phenotype of Arr11
Arr25 is a suppressor of rhabdomere phenotype of trp9
Arr25 is a suppressor | partially of rhabdomere phenotype of trp14
Arr25 is a suppressor | partially of retina phenotype of ninaEpp100
Arr25 is a suppressor | partially of rhabdomere phenotype of ninaEpp100
Arr25/Gαq1 is a suppressor of retina phenotype of ninaEpp100
Arr25 is a suppressor of rhabdomere R2 phenotype of norpAEE5
Arr25 is a suppressor of rhabdomere R3 phenotype of norpAEE5
Arr25 is a suppressor of rhabdomere R4 phenotype of norpAEE5
Arr25 is a suppressor of rhabdomere R5 phenotype of norpAEE5
Arr25 is a suppressor of rhabdomere R6 phenotype of norpAEE5
Arr25 is a suppressor of rhabdomere R1 phenotype of norpAEE5
Arr25 is a suppressor of photoreceptor cell R1 phenotype of rdgB5
Arr25 is a suppressor of photoreceptor cell R2 phenotype of rdgB5
Arr25 is a suppressor of photoreceptor cell R3 phenotype of rdgB5
Arr25 is a suppressor of photoreceptor cell R4 phenotype of rdgB5
Arr25 is a suppressor of photoreceptor cell R5 phenotype of rdgB5
Arr25 is a suppressor of photoreceptor cell R6 phenotype of rdgB5
Arr25 is a suppressor of photoreceptor neuron phenotype of rdgB5
The termination speed of photoresponses in Camtates-2; Arr25 double mutants is much slower than those of either single mutant.
Arr25 partially suppresses the retinal degeneration seen in trp14 or trp9 single mutant flies when they are maintained under a 12 hour light-12 hour dark cycle; the double mutants contain the normal number of rhabdomeres at 14 days after eclosion, although the size of the rhabdomeres is reduced compared to controls.
Light-induced currents of Arr25, ninaEpp100 double mutant photoreceptor cells show a large increase in light sensitivity relative to ninaEpp100 cells, the sensitivity is significantly less than wild-type cells. Arr25, ninaEpp100 photoreceptors produce anomalous constitutive currents in the dark, like ninaEpp100 single mutant photoreceptors. In Arr25, ninaEpp100 double mutants, retinal degeneration is significantly slowed but not abolished, when flies are kept in either constant light or constant darkness.
Gα49B1; Arr25, ninaEpp100 triple mutants show a suppression of the retinal degeneration phenotypes seen in ninaEpp100 single mutants. The triple mutants exhibit only very minor rhabdomeric abnormalities after 40 days.
norpA7, Arr25 double mutants completely rescue the degeneration observed in individual mutant and result in an ommatidial structure that closely resembles wild-type. The a light dependant retinal degeneration phenotype seen in rdgB5 is partially rescued by Arr25. The a light dependant retinal degeneration phenotype seen in Arr25 is not rescued by BacA\p35GMR.PH.