The electroantennograms of homozygous and rdgA1/rdgA3 animals show a significant decrease in amplitude compared to controls in response to a number of odours (ethyl acetate, butanol, propionic acid, benzaldehyde and iso-amyl acetate), whereas the response of heterozygotes is close to normal.
Mutants have normal antennal morphology even 6 days after eclosion.
Photoreceptors in the eye appear ultrastructurally normal in mutant flies on eclosion, but degenerate over time.
rdgA3 flies have an abnormal electroretinogram, showing a pronounced decrease in the rate of deactivation of the light response following a 1 second stimulus of light. Photoreceptors in rdgA3/+ flies also show a small but significant defect in deactivation of the light response following a 1 second stimulus of light.
Newly eclosed flies have a near-wild type ommatidium morphology, with all seven rhabdomeres being distinctly visible. Progressive degeneration is seen in all six outer rhabdomeres ver time, so that at 25[o]C, but 72 hours after eclosion, only the central R7 ommatidium can be seen. Raising flies in complete darkness throughout development does not suppress the retinal degeneration. However, the rate of degeneration is significantly higher in flies grown on a 12 hours light-dark cycle compared to flies grown in complete darkness.
Robust light responses can be recorded from mutant photoreceptors, but quantum bumps can not be detected.
Photoreceptor cells undergo severe degeneration in homozygous flies.
Rhabdomeres and photoreceptor cell bodies degenerate gradually after eclosion. Retinal degeneration starts with the disappearance of SRC. Ocellar photoreceptors also degenerate and degeneration of the SRC is observed.
Homozygous larvae are negatively photokinetic with a stimulus indice significantly higher than wild type control.
Shows abnormal localisation of anti-RDGA protein in adult photoreceptors.
The retinula cell somata and the synaptic plexus of the ocelli are normal in newly emerged flies. Extracellular debris accumulates under the ocellar retina in aged flies.
Flies show the normal arrangement of photoreceptors on the first day after pupal emergence, but by 7 days after eclosion the R1-R6 cells are noticeably disoriented (the R7 and R8 cells are less affected). The lamina and medulla appear to degenerate less than the retina. The electroretinogram (ERG) R1-R6 waveform is smaller than wild-type in a rdgA3 fly aged 6 hours, and is unrecordable in a rdgA3 fly aged 72 hours. The R7/R8 ERG waveform does not alter much from pupal emergence to 72 hours after eclosion. The M-potential and on-transient is normal in a newly emerged rdgA3 fly, although neither can be elicited in flies aged 72 hours. The prolonged polarising afterpotential is transient in rdgA3 flies aged 6 hours. The ocellar ERG decreases in older flies. Phototaxis due to R7/R8 function is impaired.
rdgA3 has abnormal neurophysiology | dominant phenotype, enhanceable by Scer\GAL4ninaE.PT/lazaUAS.GFP
rdgA3 has abnormal neurophysiology phenotype, suppressible by Galpha49B[+]/Gαq221c
rdgA3 has abnormal neurophysiology phenotype, suppressible by Gα49B[+]/Gαq1370
rdgA3 has abnormal neurophysiology phenotype, suppressible by GαqRNAi.UAS.1f1/Scer\GAL4Gαq.PS
rdgA3 has abnormal neurophysiology phenotype, suppressible by laza22
rdgA3 is a suppressor of abnormal neurophysiology phenotype of Gαq1
rdgA3 has eye photoreceptor cell phenotype, enhanceable by Scer\GAL4ninaE.PT/lazaUAS.GFP
rdgA3 has eye photoreceptor cell phenotype, enhanceable by wunUAS.cZa/Scer\GAL4ninaE.PT
rdgA3 has eye photoreceptor cell phenotype, enhanceable by wun2UAS.cHa/Scer\GAL4ninaE.PT
rdgA3 has eye photoreceptor cell phenotype, enhanceable by CG11426UAS.GFP/Scer\GAL4ninaE.PT
rdgA3 has retina phenotype, enhanceable by Scer\GAL4ninaE.PT/lazaUAS.GFP
rdgA3 has eye photoreceptor cell phenotype, enhanceable by Cds1
rdgA3 has eye photoreceptor cell phenotype, enhanceable by sktlΔ1-1/sktlΔ20
rdgA3 has phenotype, suppressible by su(rdgA)4040
rdgA3 has eye photoreceptor cell phenotype, suppressible by laza22/laza22
rdgA3 has eye photoreceptor cell phenotype, suppressible by laza[+]/laza22
rdgA3 has rhabdomere phenotype, suppressible by norpAP24
rdgA3 has rhabdomere phenotype, suppressible by Gαq1
rdgA3 has eye photoreceptor cell phenotype, non-suppressible by wunk16806/wunk12382
rdgA3 has eye photoreceptor cell phenotype, non-suppressible by wun2EP2650ex34
rdgA3 has photoreceptor neuron phenotype, non-suppressible by inaC5
rdgA3 is an enhancer of eye photoreceptor cell phenotype of Cds1
rdgA3 is a suppressor of photoreceptor neuron phenotype of Gαq1
Introduction of a single copy of Gα49B221c or Gα49B1370 to rdgA3 homozygotes significantly rescues the electroantennogram responses of the homozygotes.
Expression of Gα49BdsRNA.Scer\UAS.1f1 under the control of Scer\GAL4Gα49B.PS in rdgA3 homozygotes significantly rescues the electroantennogram responses of the homozygotes.
The rate of retinal degeneration seen in rdgA3 flies is enhanced if they are also expressing one of lazaScer\UAS.T:Avic\GFP, wunScer\UAS.cZa or wun2Scer\UAS.cHa under the control of Scer\GAL4ninaE.PT.
The rate of photoreceptor degeneration seen in rdgA3 flies is not slowed if they also carry wunk12382/wunk16806 or wun2EP2650ex34.
When CG11426Scer\UAS.T:Avic\GFP is expressed under the control of Scer\GAL4ninaE.PT in rdgA3 flies, obvious degeneration is seen in the rhabdomeres of newly eclosed flies.
When CG11426Scer\UAS.T:Avic\GFP is expressed under the control of Scer\GAL4ninaE.PT in rdgA3 norpA36 flies, the rhabdomeres are normal and do not show degeneration over time.
rdgA3 ; laza22 double mutant adults show photoreceptor degeneration in dim light, with the rate of degeneration being similar to that seen in rdgA3 single mutants. When flies are raised in bright light, the rate of photoreceptor degeneration in rdgA3 ; laza22/laza22 double mutants is greatly reduced compared to that seen in rdgA3 single mutants. The rate of photoreceptor degeneration in rdgA3 ; laza22/+ flies in bright light is intermediate between that of rdgA3 ; laza22/laza22 and rdgA3 flies.
The decreased rate of deactivation of the light response that is seen in the electroretinogram response of rdgA3 flies following a 1 second stimulus of light is substantially rescued by laza22.
The deactivation defect seen in the electroretinogram response of rdgA3/+ flies following a 1 second stimulus of light is enhanced by expression of lazaScer\UAS.T:Avic\GFP under the control of Scer\GAL4ninaE.PT.
rdgA3 ; CdsA1 double mutant flies show a higher rate of photoreceptor degeneration when raised in bright light than either rdgA3 or CdsA1 single mutants.
sktlΔ1-1/sktlΔ20 enhances the rate of photoreceptor degeneration in rdgA3 mutants.
The photoreceptor degeneration phenotype is not alleviated by the inaC5 mutation in double mutant flies.
Alleles can be ranked with respect to how much R7 and R8 are affected in each mutant; rdgA1 = rdgA2 > rdgA4 > rdgA3.