Allele Dmel\rdgC³⁰⁶

General Information
Symbol	Dmel\rdgC³⁰⁶	Species	D. melanogaster
Name		FlyBase ID	FBal0032562
Feature type	allele	Associated gene	Dmel\rdgC

Allele class	loss of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
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FB2013_03	Genes rdgC
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	loss of function allele (Steele and O'Tousa, 1990)
Mutagen	ethyl methanesulfonate (Kurada and O'Tousa, 1995)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference
Cytology
Phenotypic Data
Phenotypic Class
	increased cell death (Kiselev et al., 2000) neurophysiology defective (Vinos et al., 1997, Lee et al., 2004) thermotaxis behavior defective (Kwon et al., 2008) visible \| recessive (Steele and O'Tousa, 1990) visual behavior defective (Davidson and Steller, 1998)
Phenotype Manifest In
	ommatidium (Kiselev et al., 2000, Sahly et al., 1994, Davidson and Steller, 1998) photoreceptor cell (Kiselev et al., 2000, Davidson and Steller, 1998) rhabdomere R1 (Kiselev et al., 2000) rhabdomere R2 (Kiselev et al., 2000) rhabdomere R3 (Kiselev et al., 2000) rhabdomere R4 (Kiselev et al., 2000) rhabdomere R5 (Kiselev et al., 2000) rhabdomere R6 (Kiselev et al., 2000)
Detailed Description
	Statement Reference rdgC[306] mutant larvae show a statistically significant increase in the preference for 18[o]C. (Kwon et al., 2008) Mutant flies show a decrease in the amplitude of the electroretinogram (ERG) compared to wild type. (Lee et al., 2004) The reduction in electroretinogram (ERG) amplitude seen in flies exposed to constant light is accelerated by rdgC³⁰⁶. (Lee and Montell, 2004) rdgC³⁰⁶ animals kept in the dark for 6 days show normal ommatidial structure and highly ordered rhabdomeric structure typical of healthy photoreceptors, but animals 6 days after a single 10 minute exposure to blue light show extensive disorganisation of ommatidial structure and morphological changes in photoreceptor cells that are characteristic of apoptosis. Vesiculation and disassembly of the rhabdomeric membrane in the R1-R6 cells, and in some cases encasement of the rhabdomere by phagocytotic cells. The rhabdomere of the UV-sensitive R7 cell is unaffected. In contrast to blue-light stimulated animals, mutants 6 days after 10 min blue immediately followed by 10 min orange light exposures are indistinguishable from unstimulated animals. Photoreceptor cells in mutants stimulated by blue light and kept in the dark for 3 days show slightly smaller rhabdomeres, but little evidence of photoreceptor pathology. In contrast, a full blown picture of apoptosis is evident after 6 days. A 10 minute pulse of orange light 3 days after blue light stimulus followed by three additional days of dark shows complete suppression of apoptosis. Mutants exposed to 10 minutes of blue light followed by 4 days of dark incubation show elimination of the Deep Pseudopupil. (Kiselev et al., 2000) Ommatidia, after light-rearing for 8 weeks, show the typical features of apoptosis: cytoplasmic condensation, nuclear chromatin condensation and relatively normal looking mitochondria. (Davidson and Steller, 1998) Light-dependent retinal degeneration. ERGs and intracellular recordings demonstrate mutant photoreceptors exhibit a notable decrease in the rate of deactivation relative to control flies. Mutants exhibit a prolonged afterpotential (PDA) defect, this is also rescued by ninaE^Δ356. (Vinos et al., 1997) Flies carrying one or two copies of ninaE⁺ exhibit retinal degradation. (Kurada and O'Tousa, 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) Ultrastructural analysis of photoreceptor degeneration demonstrates that the histological and physiological deficits result from degeneration triggered by light. (Steele and O'Tousa, 1990)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement Reference rdgC³⁰⁶ is a suppressor of thermotaxis behavior defective phenotype of norpA³⁶ (Kwon et al., 2008)
Other
Statement Reference BacA\p35^GMR.PH, rdgC³⁰⁶ has wild-type phenotype (Davidson and Steller, 1998)
Phenotype Manifest In
Enhanced by
Statement Reference Gαq¹, rdgC³⁰⁶ has ommatidium phenotype, enhanceable by Arr2¹ (Kiselev et al., 2000)
Suppressed by
Statement Reference Gαq¹, rdgC³⁰⁶ has ommatidium phenotype, suppressible by Arr2³ (Kiselev et al., 2000) rdgC³⁰⁶ has ommatidium phenotype, suppressible \| partially by shi¹ (Kiselev et al., 2000) rdgC³⁰⁶ has phenotype, suppressible by ninaE^D1 (Kurada and O'Tousa, 1995) rdgC³⁰⁶ has phenotype, suppressible by ninaE^S95F (Kurada and O'Tousa, 1995) rdgC³⁰⁶ has phenotype, suppressible by ninaE^Δ356 (Vinos et al., 1997)
Other
Statement Reference Gαq¹, rdgC³⁰⁶ has ommatidium phenotype (Kiselev et al., 2000, Kiselev et al., 2000)
Additional Comments
Genetic Interactions
Statement Reference The ability of norpA[36] to select 18[o]C is eliminated in a rdgC[306] background. (Kwon et al., 2008) The light dependant retinal degeneration seen in Gα49B¹, rdgC³⁰⁶ animals is strongly suppressed by Arr2³. The addition of Gα49B¹ and Arr2¹ to rdgC³⁰⁶ show a rapid degeneration of photoreceptor cells. The addition of rdgC³⁰⁶ to Gα49B¹ flies undergo a dramatic and rapid loss of Deep Pseudopupils (DPPs) between days 4 and 6 of days of light exposure. This phenotype is partially rescued by the addition of Arr2³, and enhanced (the numbers of DPPs start to reduce immediately on exposure to light) by the addition of Arr2¹. rdgC³⁰⁶,shi¹ mutants exposed to 10 minutes of blue light followed by 4 days of dark incubation show a partial rescue of the Deep Pseudopupil phenotype seen in rdgC³⁰⁶ flies alone. (Kiselev et al., 2000) Light-induced retinal degeneration is blocked by expression of BacA\p35^GMR.PH: photoreceptor cells and organelles are indistinguishable from wild-type. The 'walking optomotor response' for rdgC³⁰⁶/BacA\p35^GMR.PH flies is normal. (Davidson and Steller, 1998) ninaE^Δ356 suppresses the deactivation defect seen in rdgC³⁰⁶ flies. (Vinos et al., 1997) Flies carrying ninaE⁺/ninaE^D1 or ninaE⁺/ninaE^D2 do not show retinal degradation. (Kurada and O'Tousa, 1995)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	rdgC³⁰⁶ is rescued by rdgC^+t7.0 (Kwon et al., 2008)
Comments
Stocks ( 1 )
Bloomington	3601 w¹¹¹⁸; rdgC³⁰⁶ kar¹ ry¹/TM3, Sb¹ Ser¹
Notes on Origin
Discoverer

Comments
	No rdgC protein is detected by antibody staining in rdgC³⁰⁶ mutants. (Steele et al., 1992)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	rdgC³⁰⁶ (Kwon et al., 2008, Wang et al., 2008, Liu et al., 2008, Shen et al., 2011)
Name Synonym
Secondary FlyBase IDs

References ( 16 )
Research paper	Shen et al., 2011, Science 331(6022): 1333--1336 Function of rhodopsin in temperature discrimination in Drosophila. [FBrf0213227] Kwon et al., 2008, Nat. Neurosci. 11(8): 871--873 Control of thermotactic behavior via coupling of a TRP channel to a phospholipase C signaling cascade. [FBrf0205753] Liu et al., 2008, Neuron 59(5): 778--789 Ca2+-dependent metarhodopsin inactivation mediated by calmodulin and NINAC myosin III. [FBrf0205960] Wang et al., 2008, J. Neurosci. 28(6): 1444--1451 Role of protein phosphatase 2A in regulating the visual signaling in Drosophila. [FBrf0202809] Lee et al., 2004, Proc. Natl. Acad. Sci. U.S.A. 101(32): 11874--11879 Rhodopsin kinase activity modulates the amplitude of the visual response in Drosophila. [FBrf0180623] Lee and Montell, 2004, Curr. Biol. 14(23): 2076--2085 Suppression of constant-light-induced blindness but not retinal degeneration by inhibition of the rhodopsin degradation pathway. [FBrf0183812] Kiselev et al., 2000, Neuron 28(1): 139--152 A molecular pathway for light-dependent photorecptor apoptosis in Drosophila. [FBrf0131331] Davidson and Steller, 1998, Nature 391(6667): 587--591 Blocking apoptosis prevents blindness in Drosophila retinal degeneration mutants. [FBrf0100553] Vinos et al., 1997, Science 277(5326): 687--690 A G protein-coupled receptor phosphatase required for rhodopsin function. [FBrf0097694] Kurada and O'Tousa, 1995, Neuron 14(3): 571--579 Retinal degeneration caused by dominant rhodopsin mutations in Drosophila. [FBrf0080181] Sawin-McCormack et al., 1995, J. Neurogenet. 10(2): 119--135 Characterization and genetic analysis of Drosophila melanogaster photobehavior during larval development. [FBrf0085888] Sahly et al., 1994, Vis. Neurosci. 11(4): 763--772 Accumulation of calcium in degenerating photoreceptors of several Drosophila mutants. [FBrf0074339] Byk et al., 1993, Proc. Natl. Acad. Sci. U.S.A. 90(5): 1907--1911 Regulatory arrestin cycle secures the fidelity and maintenance of the fly photoreceptor cell. [FBrf0059241] Steele et al., 1992, Cell 69: 669--676 Drosophila retinal degeneration C (rdgC) encodes a novel serine/threonine protein phosphatase. [FBrf0055577] Steele and O'Tousa, 1990, Neuron 4: 883--890 Rhodopsin activation causes retinal degeneration in Drosophila rdgC mutant. [FBrf0052690]
Review	Jacobson, 1998, Curr. Biol. 8(12): R418--R421 Anti-apoptosis therapy: a way of treating neural degeneration? [FBrf0104828]

Allele Dmel\rdgC306

Allele Dmel\rdgC³⁰⁶