Allele Dmel\rdgA¹

General Information
Symbol	Dmel\rdgA¹	Species	D. melanogaster
Name		FlyBase ID	FBal0014457
Feature type	allele	Associated gene	Dmel\rdgA
Also Known As	rdgA^BS12

Map ( GBrowse )
Allele class
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	ethyl methanesulfonate (Inoue et al., 1989, Masai et al., 1993, Masai et al., 1997)
Mutations Mapped to the Genome

Type Location Additional Notes References point mutation X:8,915,781..8,915,781 evidence=experimental comment=Position of mutation on reference sequence inferred by FlyBase curator based on author statement. reported_pr_change=Q1153@ pr_change=Q1156@\|rdgA-PA reported_na_change=C3695T na_change=C8915781T (Masai et al., 1993)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name D17315

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Nucleotide substitution: C3695T. Nonsense mutation corresponds to residue 1153 which is located between the catalytic domain and ankyrin repeats. (Masai et al., 1993)
Cytology
Phenotypic Data
Phenotypic Class
	auditory perception defective \| adult stage (Senthilan et al., 2012) neurophysiology defective (Kwon and Montell, 2006, Kain et al., 2008) neurophysiology defective (with rdgA³) (Kain et al., 2008) neurophysiology defective \| adult stage (Senthilan et al., 2012) visible (Georgiev et al., 2005)
Phenotype Manifest In
	eye (Kwon and Montell, 2006, Georgiev et al., 2005) ocellus (Stark et al., 1989) ocellus rhabdomere (Stark et al., 1989) ommatidium (Raghu et al., 2000) ommatidium & microvillus (Raghu et al., 2000) photoreceptor cell (Inoue et al., 1989) 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 (Harris and Stark, 1977, Masai et al., 1997) photoreceptor cell R8 (Harris and Stark, 1977, Masai et al., 1997) retina (Johnson et al., 1982, Georgiev et al., 2005) rhabdomere (Kwon and Montell, 2006, Georgiev et al., 2005)
Detailed Description
	Statement Reference 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 rdgA[1]/rdgA[3] 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[1] 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
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference rdgA¹ has neurophysiology defective phenotype, suppressible \| partially by laza¹ (Kwon and Montell, 2006) rdgA¹ has neurophysiology defective phenotype, suppressible by Galpha49B[+]/Gαq^221c (Kain et al., 2008) rdgA¹ has neurophysiology defective phenotype, suppressible by Gα49B[+]/Gαq¹³⁷⁰ (Kain et al., 2008) rdgA¹ has neurophysiology defective phenotype, suppressible by Gαq^{dsRNA.Scer\UAS.1f1}/Scer\GAL4^Gα49B.PS (Kain et al., 2008) rdgA¹ has visible phenotype, suppressible \| somatic clone by inaD^su1 (Georgiev et al., 2005) rdgA¹ has visible phenotype, suppressible \| somatic clone by inaD^su100 (Georgiev et al., 2005) rdgA¹ has visible phenotype, suppressible \| somatic clone by su(rdgA)40⁴⁰ (Georgiev et al., 2005) rdgA¹ has visible phenotype, suppressible by trp⁹ (Georgiev et al., 2005)
Suppressor of
Statement Reference rdgA¹ is a suppressor of neurophysiology defective phenotype of norpA³³ (Hardie et al., 2002) rdgA¹ is a suppressor of neurophysiology defective phenotype of norpA³⁵ (Hardie et al., 2002)
Phenotype Manifest In
Suppressed by
Statement Reference rdgA¹ has eye phenotype, suppressible \| partially by laza¹ (Kwon and Montell, 2006) rdgA¹ has eye phenotype, suppressible \| somatic clone by inaD^su1 (Georgiev et al., 2005) rdgA¹ has eye phenotype, suppressible \| somatic clone by inaD^su100 (Georgiev et al., 2005) rdgA¹ has eye phenotype, suppressible \| somatic clone by su(rdgA)40⁴⁰ (Georgiev et al., 2005) rdgA¹ has eye phenotype, suppressible by trp⁹ (Georgiev et al., 2005) rdgA¹ has ommatidium & microvillus phenotype, suppressible \| partially by trp¹ (Raghu et al., 2000) rdgA¹ has ommatidium & microvillus phenotype, suppressible \| partially by trp² (Raghu et al., 2000) rdgA¹ has ommatidium & microvillus phenotype, suppressible \| partially 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 \| partially by trp¹ (Raghu et al., 2000) rdgA¹ has ommatidium phenotype, suppressible \| partially by trp² (Raghu et al., 2000) rdgA¹ has ommatidium phenotype, suppressible \| partially 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 \| partially by trp¹ (Raghu et al., 2000) rdgA¹ has phenotype, suppressible \| partially by trp² (Raghu et al., 2000) rdgA¹ has phenotype, suppressible \| partially by trp⁹ (Raghu et al., 2000) rdgA¹ has retina phenotype, suppressible by Df(2R)BSC29/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)w45-19g/su(rdgA)40⁵ (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 Df(2R)w45-19g/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)40⁵/su(rdgA)40⁴⁰ (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 su(rdgA)40⁸/su(rdgA)40⁸ (Georgiev et al., 2012) rdgA¹ has retina phenotype, suppressible by su(rdgA)40⁴⁰ (Georgiev et al., 2012) rdgA¹ has rhabdomere phenotype, suppressible \| partially by laza¹ (Kwon and Montell, 2006) rdgA¹ has rhabdomere phenotype, suppressible \| somatic clone by inaD^su1 (Georgiev et al., 2005) rdgA¹ has rhabdomere phenotype, suppressible \| somatic clone by su(rdgA)40⁴⁰ (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^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^T2 (Georgiev et al., 2005) rdgA¹ has rhabdomere phenotype, suppressible by norpA³³ (Georgiev et al., 2005) rdgA¹ has rhabdomere phenotype, suppressible by norpA³⁵ (Georgiev et al., 2005) rdgA¹ has rhabdomere phenotype, suppressible by norpA³⁶ (Georgiev et al., 2005)
NOT suppressed by
Statement Reference rdgA¹ has phenotype, non-suppressible by trpl³⁰² (Raghu et al., 2000) rdgA¹ has retina phenotype, non-suppressible by inaC⁵ (Masai et al., 1997) rdgA¹ has rhabdomere phenotype, non-suppressible by inaD^P215 (Georgiev et al., 2005) rdgA¹ has rhabdomere phenotype, non-suppressible by ninaE¹⁷ (Georgiev et al., 2005) rdgA¹ has rhabdomere phenotype, non-suppressible by trp¹/trp^Δ1272 (Georgiev et al., 2005)
Suppressor of
Statement Reference rdgA¹ is a suppressor of photoreceptor cell phenotype of norpA³³ (Hardie et al., 2002) rdgA¹ is a suppressor of photoreceptor cell phenotype of norpA³⁵ (Hardie et al., 2002)
Additional Comments
Genetic Interactions
Statement Reference su(rdgA)40[40] can block the retinal degeneration seen in rdgA[1] mutant eyes for up to 10 days post eclosion. (Georgiev et al., 2012) Introduction of a single copy of Gα49B[221c] or Gα49B[1370] to rdgA[1] 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[1] 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 rdgA[1] flies is suppressed by trp[9] (as assayed by the presence of a crisp pseudopupil in the double mutant flies). The retinal degeneration phenotype of rdgA[1] flies is suppressed if the eyes are also composed entirely of homozygous inaD[su1], inaD[su100] or su(rdgA)40[40] tissue (clones generated using the EGUF method). The retinal degeneration phenotype of rdgA[1] flies is suppressed by inaD[T1], inaD[T1]/inaD[su1] and inaD[T1]/inaD[su100]. The retinal degeneration phenotype of rdgA[1] flies is suppressed by inaD[T2]. The retinal degeneration phenotype of rdgA[1] flies is not suppressed by inaD[P215] or ninaE[17]. rdgA[1] ; trp[1], trp[Δ1272] flies so not show suppression of the rdgA[1] retinal degeneration phenotype. norpA[36], norpA[33] and norpA[35] each almost completely suppress the retinal degeneration seen in rdgA[1] 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 & Rescue Data
Rescued by	rdgA¹ is rescued by rdgA^{ninaE.DGK2.ΔAK} (Masai et al., 1997) rdgA¹ is rescued by rdgA^ninaE.DGK2 (Masai et al., 1997)
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

Comments
	rdgA¹ flies lack diacylglycerol kinase activity in a gene dosage-dependent manner, suggesting that rdgA codes for diacylglycerol kinase. (Inoue et al., 1989) 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)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	rdgA1 (Georgiev et al., 2012) rdgA¹ (Georgiev et al., 2005, Kain et al., 2008, Senthilan et al., 2012) rdgA^BS12 (Raghu et al., 2000, Masai et al., 1997, Sawin-McCormack et al., 1995, Masai et al., 1993, Johnson et al., 1982, Stark et al., 1989, Inoue et al., 1989, Harris and Stark, 1977, Kwon and Montell, 2006, Kwon and Montell, 2006)
Name Synonym
Secondary FlyBase IDs

References ( 20 )
Research paper	Georgiev et al., 2012, J. Neurogenet. 26(3-4): 338--347 Identification of a suppressor of retinal degeneration in Drosophila photoreceptors. [FBrf0220084] Senthilan et al., 2012, Cell 150(5): 1042--1054 Drosophila auditory organ genes and genetic hearing defects. [FBrf0219321] Kain et al., 2008, J. Neurosci. 28(18): 4745--4755 Reduced odor responses from antennal neurons of G(q)alpha, phospholipase Cbeta, and rdgA mutants in Drosophila support a role for a phospholipid intermediate in insect olfactory transduction. [FBrf0204625] Kwon and Montell, 2006, Curr. Biol. 16(7): 723--729 Dependence on the Lazaro phosphatidic acid phosphatase for the maximum light response. [FBrf0190027] Georgiev et al., 2005, J. Cell Sci. 118(Pt 7): 1373--1384 Functional INAD complexes are required to mediate degeneration in photoreceptors of the Drosophila rdgA mutant. [FBrf0184068] Hardie et al., 2004, J. Biol. Chem. 279(46): 47773--47782 In vivo light-induced and basal phospholipase C activity in Drosophila photoreceptors measured with genetically targeted phosphatidylinositol 4,5-bisphosphate-sensitive ion channels (Kir2.1). [FBrf0179836] Hardie et al., 2003, J. Biol. Chem. 278(21): 18851--18858 Rescue of light responses in the Drosophila 'null' phospholipase C mutant, norpA[P24], by the diacylglycerol kinase mutant, rdgA, and by metabolic inhibition. [FBrf0159791] Hardie et al., 2002, Neuron 36(4): 689--701 Molecular basis of amplification in Drosophila phototransduction. Roles for g protein, phospholipase C, and diacylglycerol kinase. [FBrf0152274] Raghu et al., 2000, Neuron 26(1): 169--179 Constitutive activity of the light-sensitive channels TRP and TRPL in the Drosophila diacylglycerol kinase mutant, rdgA. [FBrf0127286] Masai et al., 1997, J. Neurobiol. 32(7): 695--706 Immunolocalization of Drosophila eye-specific diacylgylcerol kinase, rdgA, which is essential for the maintenance of the photoreceptor. [FBrf0093591] Gordesky-Gold et al., 1995, Genetics 139(4): 1623--1629 Hypomorphic mutations in the larval photokinesis A, lphA, gene have stage-specific effects on visual system function in Drosophila melanogaster. [FBrf0080060] Sawin-McCormack et al., 1995, J. Neurogenet. 10(2): 119--135 Characterization and genetic analysis of Drosophila melanogaster photobehavior during larval development. [FBrf0085888] Masai et al., 1993, Proc. Natl. Acad. Sci. U.S.A. 90(23): 11157--11161 Drosophila retinal degeneration A gene encodes an eye-specific diacylglycerol kinase with cysteine-rich zinc-finger motifs and ankyrin repeats. [FBrf0064600] Inoue et al., 1989, J. Biol. Chem. 264: 5996--6000 Diacylglycerol kinase defect in a Drosophila retinal degeneration mutant rdgA. [FBrf0050148] Stark et al., 1989, J. Neurogenet. 5: 127--153 Ultrastructure of the ocellar visual system in normal and mutant Drosophila melanogaster. [FBrf0050358] Johnson et al., 1982, J. Insect Physiol. 28(3): 233--242 Characterization of rdgA: mutants with retinal degeneration in Drosophila. [FBrf0064896] Harris and Stark, 1977, J. Gen. Physiol. 69: 261--291 Hereditary retinal degeneration in Drosophila melanogaster. A mutant defect associated with the phototransduction process. [FBrf0030443] Hotta and Benzer, 1970, Proc. Natl. Acad. Sci. U.S.A. 67: 1156--1163 Genetic dissection of the Drosophila nervous system by means of mosaics. [FBrf0021930]
Supplementary material	Kwon and Montell, 2006, Curr. Biol. 16(7): Supplemental data. [FBrf0199312]
Abstract	Masai et al., 1993, Davis, Zipursky, 1993: 172 Molecular cloning of Drosophila retinal degeneration A (rdgA) gene: an eye-specific diacylglycerol kinase with ankyrin repeats. [FBrf0078978]

Allele Dmel\rdgA1

Allele Dmel\rdgA¹