FlyBase Allele Report: Dmel\rdgA[1]

FB2025_01 , released February 20, 2025

FB2025_01 , released February 20, 2025

Allele: Dmel\rdgA¹

General Information

Symbol

Dmel\rdgA¹

Species

D. melanogaster

Name

FlyBase ID

FBal0014457

Feature type

allele

Associated gene

Associated Insertion(s)

Carried in Construct

Also Known As

rdgA^BS12

Key Links

Genomic Maps

Allele class

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

Mutagen

ethyl methanesulfonate

(Masai et al., 1997, Masai et al., 1993, Inoue et al., 1989)

Progenitor genotype

Cytology

Description

Nucleotide substitution G3677A in transcript A of rdgA, corresponding to an amino acid substitution of G900S in this isoform (stated to be a revision of data in FBrf0064600).

(Ogueta et al., 2020.5.7)

Nucleotide substitution: C3695T. Nonsense mutation corresponds to residue 1153 which is located between the catalytic domain and ankyrin repeats.

(Masai et al., 1993)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

X:9,019,990..9,019,990 [+]

Nucleotide change:

G9019990A

Amino acid change:

G900S | rdgA-PA; G452S | rdgA-PB; G467S | rdgA-PC; G434S | rdgA-PD; G434S | rdgA-PE; G895S | rdgA-PG; G900S | rdgA-PH; G903S | rdgA-PI; G900S | rdgA-PJ; G900S | rdgA-PK; G900S | rdgA-PL

Reported amino acid change:

G900S

Comment:

rdgA[1] sequence reported by Maite Ogueta published in biorxiv, DOI 10.1101/2020.03.10.985044, shows a mutation resulting in a G900S amino acid change and not the Q1161term originally reported by Masai et al. 1993.

(Ogueta et al., 2020.5.7)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

Disease

Interaction

References

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal auditory perception | adult stage

(Senthilan et al., 2012)

abnormal neurophysiology

(Kain et al., 2008, Kwon and Montell, 2006)

abnormal neurophysiology (with rdgA³)

(Kain et al., 2008)

abnormal neurophysiology | adult stage

(Senthilan et al., 2012)

increased cell death | adult stage | progressive

(Huang et al., 2015)

(Georgiev et al., 2005)

Phenotype Manifest In

(Kwon and Montell, 2006, Georgiev et al., 2005)

eye | progressive

(Huang et al., 2015)

eye photoreceptor cell | progressive

(Huang et al., 2015)

(Stark et al., 1989)

ocellus rhabdomere

(Stark et al., 1989)

(Raghu et al., 2000)

ommatidium & microvillus

(Raghu et al., 2000)

photoreceptor cell R1

(Masai et al., 1997, Johnson et al., 1982)

photoreceptor cell R2

(Masai et al., 1997, Johnson et al., 1982)

photoreceptor cell R3

(Masai et al., 1997, Johnson et al., 1982)

photoreceptor cell R4

(Masai et al., 1997, Johnson et al., 1982)

photoreceptor cell R5

(Masai et al., 1997, Johnson et al., 1982)

photoreceptor cell R6

(Masai et al., 1997, Johnson et al., 1982)

photoreceptor cell R7

(Masai et al., 1997, Harris and Stark, 1977)

photoreceptor cell R8

(Masai et al., 1997, Harris and Stark, 1977)

photoreceptor neuron

(Inoue et al., 1989)

(Georgiev et al., 2005, Johnson et al., 1982)

retina | progressive

(Huang et al., 2015)

(Kwon and Montell, 2006, Georgiev et al., 2005)

rhabdomere of eye photoreceptor cell | progressive

(Huang et al., 2015)

Detailed Description

Statement

Reference

The integrity of photoreceptor cells (including loss of rhabdomere structures in the retina) degenerates in rdgA¹/rdgA¹ 5 day old flies (compared to 1 day old).

(Huang et al., 2015)

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.

(Senthilan et al., 2012)

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. The kinetics of the termination of the electroantennogram response is normal in rdgA¹ homozygotes.

Mutants have normal antennal morphology even 6 days after eclosion.

(Kain et al., 2008)

The number and size of the rhabdomeres is dramatically reduced in 1-day-old rdgA¹ flies.

(Kwon and Montell, 2006)

Mutant flies show a retinal degeneration phenotype, which is unaffected by dark rearing.

(Georgiev et al., 2005)

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.

(Raghu et al., 2000)

Photoreceptor cells undergo severe degeneration in homozygous flies. This phenotype is rescued in the outer photoreceptor cells (R1-R6) in homozygous flies carrying rdgA^ninaE.DGK2 or rdgA^{ninaE.DGK2.ΔAK}.

(Masai et al., 1997)

Homozygous larvae are negatively photokinetic with a stimulus indice significantly higher than wild type control and transheterozygotes with lphA² have a lower indice.

(Gordesky-Gold et al., 1995)

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.

(Sawin-McCormack et al., 1995)

Photoreceptor degeneration occurs during the first week of adult life. Diacylglycerol kinase activity is very low compared to wild-type.

(Inoue et al., 1989)

The ocelli of newly emerged flies contain few if any rhabdomeric microvilli, and there is extracellular debris in the ocellar retina of aged flies.

(Stark et al., 1989)

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.

(Johnson et al., 1982)

Photoreceptors R7 and R8 are preserved in less than 10% of ommatidia in 7 day old mutant flies.

(Harris and Stark, 1977)

External Data

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

rdgA¹ has abnormal neurophysiology phenotype, suppressible by Galpha49B[+]/Gαq^221c

(Kain et al., 2008)

rdgA¹ has abnormal neurophysiology phenotype, suppressible by Gα49B[+]/Gαq¹³⁷⁰

(Kain et al., 2008)

rdgA¹ has abnormal neurophysiology phenotype, suppressible by Gαq^RNAi.UAS.1f1/Scer\GAL4^Gαq.PS

(Kain et al., 2008)

rdgA¹ has abnormal neurophysiology phenotype, suppressible by laza¹

(Kwon and Montell, 2006)

rdgA¹ has visible phenotype, suppressible by trp⁹

(Georgiev et al., 2005)

rdgA¹ has visible phenotype, suppressible by su(rdgA)40⁴⁰

(Georgiev et al., 2005)

rdgA¹ has visible phenotype, suppressible by inaD^su100

(Georgiev et al., 2005)

rdgA¹ has visible phenotype, suppressible by inaD^su1

(Georgiev et al., 2005)

Suppressor of

Statement

Reference

rdgA¹ is a suppressor of abnormal neurophysiology phenotype of norpA^P12

(Hardie et al., 2002)

rdgA¹ is a suppressor of abnormal neurophysiology phenotype of norpA^P16

(Hardie et al., 2002)

Phenotype Manifest In

Suppressed by

Statement

Reference

rdgA¹ has retina phenotype, suppressible by su(rdgA)40⁴⁰

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by Df(2R)w45-19g/su(rdgA)40⁴⁰

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by Df(2R)Np5/su(rdgA)40⁴⁰

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by Df(2R)BSC29/su(rdgA)40⁴⁰

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by Df(2R)w45-19g/su(rdgA)40⁵

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by su(rdgA)40⁵/su(rdgA)40⁴⁰

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by su(rdgA)40⁵/su(rdgA)40⁵

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by su(rdgA)40⁶/Df(2R)w45-19g

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by su(rdgA)40⁶/su(rdgA)40⁶

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by Df(2R)w45-19g/su(rdgA)40⁸

(Georgiev et al., 2012)

rdgA¹ has retina phenotype, suppressible by su(rdgA)40⁸/su(rdgA)40⁸

(Georgiev et al., 2012)

rdgA¹ has rhabdomere phenotype, suppressible by laza¹

(Kwon and Montell, 2006)

rdgA¹ has eye phenotype, suppressible by laza¹

(Kwon and Montell, 2006)

rdgA¹ has eye phenotype, suppressible by trp⁹

(Georgiev et al., 2005)

rdgA¹ has eye phenotype, suppressible by su(rdgA)40⁴⁰

(Georgiev et al., 2005)

rdgA¹ has eye phenotype, suppressible by inaD^su100

(Georgiev et al., 2005)

rdgA¹ has eye phenotype, suppressible by inaD^su1

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by su(rdgA)40⁴⁰

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by inaD^su1

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by inaD^T1

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by inaD^T1/inaD^su1

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by inaD^su100/inaD^T1

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by inaD^T2

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by norpA^P24

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by norpA^P16

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, suppressible by norpA^P12

(Georgiev et al., 2005)

rdgA¹ has phenotype, suppressible by trp²

(Raghu et al., 2000)

rdgA¹ has phenotype, suppressible by trp⁹

(Raghu et al., 2000)

rdgA¹ has ommatidium & microvillus phenotype, suppressible by trp¹

(Raghu et al., 2000)

rdgA¹ has ommatidium & microvillus phenotype, suppressible by trp²

(Raghu et al., 2000)

rdgA¹ has ommatidium & microvillus phenotype, suppressible by trp⁹

(Raghu et al., 2000)

rdgA¹ has ommatidium & microvillus phenotype, suppressible by trp¹/trpl³⁰²

(Raghu et al., 2000)

rdgA¹ has ommatidium & microvillus phenotype, suppressible by trp²/trpl³⁰²

(Raghu et al., 2000)

rdgA¹ has ommatidium & microvillus phenotype, suppressible by trpl³⁰²/trp⁹

(Raghu et al., 2000)

rdgA¹ has ommatidium phenotype, suppressible by trp¹

(Raghu et al., 2000)

rdgA¹ has ommatidium phenotype, suppressible by trp²

(Raghu et al., 2000)

rdgA¹ has ommatidium phenotype, suppressible by trp⁹

(Raghu et al., 2000)

rdgA¹ has ommatidium phenotype, suppressible by trp¹/trpl³⁰²

(Raghu et al., 2000)

rdgA¹ has ommatidium phenotype, suppressible by trp²/trpl³⁰²

(Raghu et al., 2000)

rdgA¹ has ommatidium phenotype, suppressible by trpl³⁰²/trp⁹

(Raghu et al., 2000)

rdgA¹ has phenotype, suppressible by trp¹

(Raghu et al., 2000)

NOT suppressed by

Statement

Reference

rdgA¹ has rhabdomere phenotype, non-suppressible by inaD^P215

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, non-suppressible by trp¹/trp^Δ1272

(Georgiev et al., 2005)

rdgA¹ has rhabdomere phenotype, non-suppressible by ninaE¹⁷

(Georgiev et al., 2005)

rdgA¹ has phenotype, non-suppressible by trpl³⁰²

(Raghu et al., 2000)

rdgA¹ has retina phenotype, non-suppressible by inaC⁵

(Masai et al., 1997)

Suppressor of

Statement

Reference

rdgA¹ is a suppressor of photoreceptor neuron phenotype of norpA^P12

(Hardie et al., 2002)

rdgA¹ is a suppressor of photoreceptor neuron phenotype of norpA^P16

(Hardie et al., 2002)

Additional Comments

Genetic Interactions

Statement

Reference

su(rdgA)40⁴⁰ can block the retinal degeneration seen in rdgA¹ mutant eyes for up to 10 days post eclosion.

(Georgiev et al., 2012)

Introduction of a single copy of Gα49B^221c or Gα49B¹³⁷⁰ to rdgA¹ 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 rdgA¹ homozygotes significantly rescues the electroantennogram responses of the homozygotes.

(Kain et al., 2008)

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.

(Kwon and Montell, 2006)

The retinal degeneration phenotype of rdgA¹ flies is suppressed by trp⁹ (as assayed by the presence of a crisp pseudopupil in the double mutant flies).

The retinal degeneration phenotype of rdgA¹ flies is suppressed if the eyes are also composed entirely of homozygous inaD^su1, inaD^su100 or su(rdgA)40⁴⁰ tissue (clones generated using the EGUF method).

The retinal degeneration phenotype of rdgA¹ flies is suppressed by inaD^T1, inaD^T1/inaD^su1 and inaD^T1/inaD^su100.

The retinal degeneration phenotype of rdgA¹ flies is suppressed by inaD^T2.

The retinal degeneration phenotype of rdgA¹ flies is not suppressed by inaD^P215 or ninaE¹⁷.

rdgA¹ ; trp¹, trp^Δ1272 flies so not show suppression of the rdgA¹ retinal degeneration phenotype.

norpA³⁶, norpA³³ and norpA³⁵ each almost completely suppress the retinal degeneration seen in rdgA¹ flies.

(Georgiev et al., 2005)

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.

(Hardie et al., 2003)

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.

(Hardie et al., 2002)

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.

(Raghu et al., 2000)

The retinal degeneration phenotype is not alleviated by the inaC⁵ mutation in double mutant flies.

(Masai et al., 1997)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

rdgA¹ is rescued by rdgA^ninaE.DGK2

(Masai et al., 1997)

rdgA¹ is rescued by rdgA^{ninaE.DGK2.ΔAK}

(Masai et al., 1997)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

Comments

Alleles can be ranked with respect to how much R7 and R8 are affected in each mutant; rdgA¹ = rdgA² > rdgA⁴ > rdgA³.

(Harris and Stark, 1977)

rdgA¹ flies lack diacylglycerol kinase activity in a gene dosage-dependent manner, suggesting that rdgA codes for diacylglycerol kinase.

(Inoue et al., 1989)

External Crossreferences and Linkouts ( 1 )

Crossreferences

GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.

D17315

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

rdgA1

(Georgiev et al., 2012)

rdgA¹

(Ogueta et al., 2020.5.7, Hardie et al., 2015, Senthilan et al., 2012, Kain et al., 2009, Kain et al., 2008, Georgiev et al., 2005)

rdgA^BS12

(Huang et al., 2015, Kwon and Montell, 2006, Kwon and Montell, 2006, Raghu et al., 2000, Masai et al., 1997, Sawin-McCormack et al., 1995, Masai et al., 1993, Inoue et al., 1989, Stark et al., 1989, Johnson et al., 1982, Harris and Stark, 1977)

Name Synonyms

Secondary FlyBase IDs

References (24)

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