Allele Dmel\Rh3^Rh1+3

General Information
Symbol	Dmel\Rh3^Rh1+3	Species	D. melanogaster
Name		FlyBase ID	FBal0030113
Feature type	allele	Associated gene	Dmel\Rh3

Allele class
Mutagen	in vitro construct - regulatory fusion
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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FB2013_03
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
Mutagen	in vitro construct - regulatory fusion (Feiler et al., 1992, Shetty et al., 1998)
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 Construct: Entire gene and upstream sequences of Rh3 are fused to 2.8kb ninaE promoter fragment containing 67 nucleotides of untranslated leader sequence. (Feiler et al., 1992)
Carried in construct	P{Rh3^Rh1+3} (Salcedo et al., 1999, Feiler et al., 1992, Shetty et al., 1998, Lee et al., 1996, Meyer et al., 2006, Liu et al., 2008)
Cytology
Phenotypic Data
Phenotypic Class
	neurophysiology defective (Liu et al., 2008)
Phenotype Manifest In
	ommatidium (Liu et al., 2008)
Detailed Description
	Statement Reference Whole-cell voltage-clamp recordings of dissociated ommatidia from flies of the genotype ninaE[17],Rh3[Rh1+3] (in which the UV responsive Rh3 is driven in place of ninaE by this latter's promoter) show similar, albeit slightly slower, kinetics to responses from wildtype ommatidia. Quantum bumps are similar in waveform, but slightly larger than wildtype, and a similar dependence on Ca[2+] is seen. (Liu et al., 2008)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference Rh3^Rh1+3 has neurophysiology defective phenotype, suppressible by ninaC⁵ (Liu et al., 2008)
NOT suppressed by
Statement Reference Rh3^Rh1+3 has neurophysiology defective phenotype, non-suppressible by ninaE¹⁷ (Liu et al., 2008)
Suppressor of
Statement Reference Rh3^Rh1+3 is a suppressor of neurophysiology defective phenotype of ninaC⁵ (Liu et al., 2008)
NOT Suppressor of
Statement Reference ninaE¹⁷/Rh3^Rh1+3 is a non-suppressor of neurophysiology defective phenotype of Arr2⁵ (Liu et al., 2008)
Other
Statement Reference Rh3^Rh1+3, ninaE¹⁷ has optomotor response defective phenotype (Yamaguchi et al., 2008)
Phenotype Manifest In
Suppressed by
Statement Reference Rh3^Rh1+3 has ommatidium phenotype, suppressible by ninaC⁵ (Liu et al., 2008)
NOT suppressed by
Statement Reference Rh3^Rh1+3 has ommatidium phenotype, non-suppressible by ninaE¹⁷ (Liu et al., 2008)
Suppressor of
Statement Reference Rh3^Rh1+3 is a suppressor of ommatidium phenotype of ninaC⁵ (Liu et al., 2008) Rh3^Rh1+3 is a suppressor of phenotype of ninaE¹⁷ (Feiler et al., 1992)
NOT Suppressor of
Statement Reference ninaE¹⁷/Rh3^Rh1+3 is a non-suppressor of ommatidium phenotype of Arr2⁵ (Liu et al., 2008)
Additional Comments
Genetic Interactions
Statement Reference In whole-cell voltage-clamp recording of dissociated ommatidia from Arr2[5] flies carrying Rh3[Rh1+3] and mutant for ninaE[17], the response to brief flashes of UV light inactivates normally but then fails to rapidly reach baseline leaving a secondary peak that decays over several seconds. Flies expressing Rh3[Rh1+3] in the ninaC[5] mutant background show that the slowly decaying tail is rapidly suppressed by photoreconversion of metarhodopsin to rhodopsin. (Liu et al., 2008) Rh3[Rh1+3], ninaE[17] flies exhibit a shift in the point of equiluminance such that, compared with wild-type flies much less blue light is required to balace the standard green intensity, giving a blue/green ratio of 0.017 compared with 0.40 for wild-type flies. (Yamaguchi et al., 2008)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	P^Rh1+3 (Yamaguchi et al., 2008) Rh3^Rh1+3
Name Synonym
Secondary FlyBase IDs

References ( 7 )
Research paper	Liu et al., 2008, Neuron 59(5): 778--789 Ca2+-dependent metarhodopsin inactivation mediated by calmodulin and NINAC myosin III. [FBrf0205960] Yamaguchi et al., 2008, Proc. Natl. Acad. Sci. U.S.A. 105(12): 4910--4915 Motion vision is independent of color in Drosophila. [FBrf0204275] Meyer et al., 2006, J. Cell Sci. 119(Pt 12): 2592--2603 Subcellular translocation of the eGFP-tagged TRPL channel in Drosophila photoreceptors requires activation of the phototransduction cascade. [FBrf0193744] Salcedo et al., 1999, J. Neurosci. 19(24): 10716--10726 Blue- and green-absorbing visual pigments of Drosophila: ectopic expression and physiological characterization of the R8 photoreceptor cell-specific Rh5 and Rh6 rhodopsins. [FBrf0123183] Shetty et al., 1998, J. Biol. Chem. 273(32): 20425--20430 Rab6 regulation of rhodopsin transport in Drosophila. [FBrf0103372] Lee et al., 1996, Microsc. Res. Tech. 35(6): 418--430 Vitamin A, visual pigments, and visual receptors in Drosophila. [FBrf0091394] Feiler et al., 1992, J. Neurosci. 12(10): 3862--3868 Ectopic expression of ultraviolet-rhodopsins in the blue photoreceptor cells of Drosophila: visual physiology and photochemistry of transgenic animals. [FBrf0056577]

Allele Dmel\Rh3Rh1+3

Allele Dmel\Rh3^Rh1+3