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General Information
Symbol
Dmel\Rh52
Species
D. melanogaster
Name
FlyBase ID
FBal0265961
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

FLPase-mediated excision of P{GT1}BG01539, located 1.2kb upstream of Rh5, and P{EP}EP574, found downstream of the Rh5 ORF.

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 ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Rh52 homozygous mutant mid and late third instar (96 and 120 hr AEL, respectively) larvae show impaired temperature selection and unlike controls display no strong preference for cooler temperatures (18[o]C) in a temperature gradient. This effect does not appear to be due to developmental delay as the mutants develop with similar timing as controls, they also do not show any gross defects in the morphology of TrpA1 neurons, 18[o]C versus 28[o]C thermotaxis or crawling speed.

Mutant larvae show normal levels of avoidance in response to green light.

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. The displacement response of the antenna over a range of sound particle velocities is linearised, indicating loss of mechanical amplification.

Light avoidance is completely lost in Rh52 mutants.

Rh52 mutant class IV dendritic arborization neurons do not exhibit any defects in light response.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference

Rh52 has abnormal phototaxis phenotype, non-enhanceable by Rh61

NOT suppressed by
Statement
Reference

Rh52 has abnormal phototaxis phenotype, non-suppressible by Rh61

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Rh52, Rh61 double homozygosity rescues the circadian rhythmicity defects of cry01 homozygotes.

The impaired thermotactic behavior characteristic for Rh52 and Rh61 single mutant late third instar larvae (120 hr AEL) does not deteriorate further in the Rh52;Rh61 double mutants.

The sound threshold required to evoke a compound action potential in the antennal nerve in response in Rh52 Rh61 double mutants is almost twice as loud as required in single mutants. Ultrastructure of the Johnston's organ sensillum appears normal in the double mutant flies.

Following a 6 hour delay in their light-dark cycle, cryb Rh52 flies show a similar delay in resynchronizing their evening activity peak as cryb flies. Triple mutant cryb Rh52 Rh61 flies resynchronize over a longer period than either the cryb single or double mutants.

Following a 6 hour delay in their light-dark cycle, cryb norpA39 flies show a longer delay in resynchronizing their evening activity peak (5-7 days) compared to cryb flies. The addition of Rh52 to this background extends the time required for resynchronization to beyond 7 days. The addition of both Rh52 and Rh61 to the cryb norpA39 background results in minimal (if any) tendency to resynchronize circadian behaviour.

Following a 6 hour advancement in their light-dark cycle, cryb norpA39 flies show a longer delay in resynchronizing their circadian behaviour (several days) compared to either single mutant. Introducing Rh52 to this background interferes more strongly with resynchronization, while the quadruple cryb norpA39 Rh52 Rh61 mutant shows the strongest phenotype.

Rh52;Rh61 double mutants are completely blind, with light avoidance being completely lost at the larval stage.

Rh52;Rh61 double mutants eclose at a similar rate as in wild-type.

Despite Rh52;Rh61 double mutants having a decreased ability to degrade tim in response to light, they are still capable of proper circadian behavior.

Wild-type larvae display differences in their LN(v) dendrite length when exposed to constant darkness versus constant light. In contrast, such light induced changes are absent in Rh52, Rh61 double mutants.

sev1, Rh52, Rh61 triple mutant flies do not have R7 cells and do not express function R8 opsins, therefore colour vision should be completely abolished. However, the blue/green intensity-response curve for these flies appears indistinguishable from wild-type.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Rh5Scer\UAS.cSa in under the control of Scer\GAL4Rh5-G in the Rh52/Rh5G transheterozygote larvae (using the intrinsic Gal4 driver in Rh5G) rescues the impaired thermotactic behavior characteristic for Rh52 mutants.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (16)