|Feature type||allele||Associated gene||Dmel\rdgA|
|Also Known As||rdgABS12|
|Map ( GBrowse )|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Nucleotide substitution: C3695T. Nonsense mutation corresponds to residue 1153 which is located between the catalytic domain and ankyrin repeats.
|Phenotype Manifest In|
ommatidium & microvillus
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. Nonlinear mechanical amplification is significantly reduced compared to wild type.
The electroantennograms of homozygous and rdgA/rdgA 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. The kinetics of the termination of the electroantennogram response is normal in rdgA homozygotes. Mutants have normal antennal morphology even 6 days after eclosion.
The number and size of the rhabdomeres is dramatically reduced in 1-day-old rdgA1 flies.
Mutant flies show a retinal degeneration phenotype, which is unaffected by dark rearing.
Adult ommatidia are smaller and less robust than wild type, resembling pupal ommatidia. Cell capacitance is reduced compared to wild type, microvilli are almost absent, and Sh channels are almost absent. A novel constitutively active small inward current, characterised by high-frequency noise, is detected. This current is mediated by trp channels. The onset of constitutive activity in ~75hr old pupae coincides with the first signs of degeneration.
Photoreceptor cells undergo severe degeneration in homozygous flies. This phenotype is rescued in the outer photoreceptor cells (R1-R6) in homozygous flies carrying rdgAninaE.DGK2 or rdgAninaE.DGK2.ΔAK.
Homozygous larvae are negatively photokinetic with a stimulus indice significantly higher than wild type control and transheterozygotes with lphA2 have a lower indice.
Third instar foraging larvae show negative photobehaviour indistinguishable from the wild-type response to light. Third instar larvae show a decrease in negative phototaxis from the onset of wandering culminating in random photobehaviour indistinguishable from the response of wild-type larvae.
Photoreceptor degeneration occurs during the first week of adult life. Diacylglycerol kinase activity is very low compared to wild-type.
The ocelli of newly emerged flies contain few if any rhabdomeric microvilli, and there is extracellular debris in the ocellar retina of aged flies.
Flies show gross retinal distortion, especially of the R1-R6 cells, on the first day after pupal emergence, and by 7 days after eclosion only remnants of the R7 and R8 cells can be seen. The lamina appears striated into cartridges and the medulla appears normal. A minimal electroretinogram (ERG) is observed only in newly emerged rdgA1 flies. M-potentials cannot be recorded from rdgA1 flies. Phototaxis due to R7/R8 function is impaired.
Photoreceptors R7 and R8 are preserved in less than 10% of ommatidia in 7 day old mutant flies.
rdgA1 has neurophysiology defective phenotype, suppressible by GαqdsRNA.Scer\UAS.1f1/Scer\GAL4Gα49B.PS
|Phenotype Manifest In|
|NOT suppressed by|
su(rdgA)40 can block the retinal degeneration seen in rdgA mutant eyes for up to 10 days post eclosion.
Introduction of a single copy of Gα49B[221c] or Gα49B to rdgA homozygotes significantly rescues the electroantennogram responses of the homozygotes. Expression of Gα49B[dsRNA.Scer\UAS.1f1] under the control of Scer\GAL4[Gα49B.PS] in rdgA homozygotes significantly rescues the electroantennogram responses of the homozygotes.
laza1 partially-suppresses the rhabdomeric degeneration associated with rdgA1. One-day post-eclosion, the average number and size of the rhabdomeres is significantly increased. By 3-days post-eclosion, the double-mutant flies retain at least as many rhabdomeres as 1-day-old rdgA1 flies. However, by 7-days post-eclosion, the rdgA1;laza1 flies display severe retinal degeneration. Consistent with this partial-suppression, the electroretinogram response in the double mutant flies is partially restored.
The retinal degeneration phenotype of rdgA flies is suppressed by trp (as assayed by the presence of a crisp pseudopupil in the double mutant flies). The retinal degeneration phenotype of rdgA flies is suppressed if the eyes are also composed entirely of homozygous inaD[su1], inaD[su100] or su(rdgA)40 tissue (clones generated using the EGUF method). The retinal degeneration phenotype of rdgA flies is suppressed by inaD[T1], inaD[T1]/inaD[su1] and inaD[T1]/inaD[su100]. The retinal degeneration phenotype of rdgA flies is suppressed by inaD[T2]. The retinal degeneration phenotype of rdgA flies is not suppressed by inaD[P215] or ninaE. rdgA ; trp, trp[Δ1272] flies so not show suppression of the rdgA retinal degeneration phenotype. norpA, norpA and norpA each almost completely suppress the retinal degeneration seen in rdgA flies.
In recordings of norpA36 rdgA1 double mutant photoreceptors, with a standard electrode solution containing nucleotide additives, the constitutive inward currents recorded immediately on establishing the whole-cell configuration are greatly enhanced compared with norpA36 single mutant photoreceptors. The spontaneous currents in the double mutant photoreceptors slowly decay, reaching a quiet base line after about 20 minutes. Towards the end of this decay, large (about 8pA) slowly terminating quantum bumps can be resolved, similar in both amplitude and kinetics to those seen in norpA36 single mutant photoreceptors without ATP. Sensitivity to light is enhanced in the double mutant photoreceptors, with bright flashes eliciting responses of up to about 200pA in amplitude before the decay of the spontaneous current and responses of up to about 400pA that decay with the slow kinetics characteristic of norpA36 after decay to base line. Spontaneous currents are abolished in norpA36 Gα49B1 double mutant and Gα49B1 norpA36 rdgA1 triple mutant photoreceptors.
The small amplitude of quantum bumps in norpA35 photoreceptors (seen when ATP is present in the intracellular solution during recordings) is increased in size to near wild-type levels if the flies are also mutant for rdgA1. The small amplitude of quantum bumps in norpA33 photoreceptors (seen when ATP is present in the intracellular solution during recordings) is increased in size to near wild-type levels if the flies are also mutant for rdgA1.
Ommatidial appearance of rdgA1 is largely restored to wild type by mutants at the trp locus, though defects detectable at the EM level remain. These residual defects are suppressed in the triple mutant with trpl302. These anatomical rescue effects are paralleled by rescue of electrophysiological defects of rdgA1 mutants and the return of light sensitivity, though restored light sensitivity is not wild type showing defects in response termination. Double rdgA1, trp mutants show age-dependent retinal degeneration.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
rdgA1 flies lack diacylglycerol kinase activity in a gene dosage-dependent manner, suggesting that rdgA codes for diacylglycerol kinase.
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 3 )|
|Secondary FlyBase IDs|
|References ( 20 )|