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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Mutation in sequenced strain: deletion (-19, coding/intron).

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Rh61 adults exhibit antennal free fluctuations with a diminished power and an altered frequency tuning compared to controls. When stimulated with pure tones, the displacement response of mutant antennae lack the characteristic nonlinear intensity scaling compared to controls. Also the amplitude and sensitivity of compound action potentials responses are reduced in mutants compared to controls. Johnston's organ function of the mutants remain uncompromised by nutrient carotenoid depletion for six generations.

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 significantly decreased green-light avoidance compared to controls.

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.

Photophobicity is unaffected in Rh61 mutants.

Rh61 mutant class IV dendritic arborization neurons do not exhibit any defects in light response.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
NOT suppressed by

Rh61 has abnormal behavior | larval stage phenotype, non-suppressible by Ggt-1Δ1523

Enhancer of
NOT Enhancer of

Rh61 is a non-enhancer of abnormal locomotor rhythm phenotype of cryb

Rh61 is a non-enhancer of abnormal phototaxis phenotype of Rh52

Suppressor of
NOT Suppressor of

Rh61 is a non-suppressor of abnormal phototaxis phenotype of Rh52

Phenotype Manifest In
Additional Comments
Genetic Interactions

Rh61, Rh52 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 reduced green-light avoidance seen in Rh61 larvae is not altered if the larvae are also mutant for Ggt-1Δ1523.

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 Rh61 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 Rh61 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 Rh61 to this background interferes more strongly with resynchronization, while the quadruple cryb norpA39 Rh52 Rh61 mutant shows the strongest phenotype.

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.

A Rh61 mutant background does not affect the ability of cryb mutants to adapt to a new phase of green light (472-603nm) and Y-FL (475-724nm).

The retrainment of ninaE17 Rh61 cryb to 6 hour delayed green light (472-603nm) and Y-FL (475-724nm) is significantly slower than that of ninaE17 cryb mutants. Indeed some flies do not adapt to the new photoperiod within 7 days.

ninaE17 Rh53 Rh61 cryb and ninaE17 Rh54 Rh61 cryb quadruple mutants are not retrained by green light (472-603nm) and Y-FL (475-724nm).

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.

R7 photoreceptors cells homozygous for pros17 and Rh61 undergo partial transformation towards an R8 photoreceptor fate, as judged by marker analysis, mapping of axonal projections, and proximo-distal positioning of nuclei.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by
Not rescued by

Expression of Rh6Scer.UAS.cVa in under the control of Scer\GAL4Rh6-G in the Rh61/Rh6G transheterozygote larvae (using the intrinsic Gal4 driver in Rh6G) rescues the impaired thermotactic behavior characteristic for Rh61 mutants. The thermal preferences defects of Rh61 mutants are also rescued by expression of Rh6Scer.UAS.cVa under the combined control of Scer\GAL4TrpA1-AB-G4 and Scer\GAL4TrpA1-CD-G4, the rescue effect is weaker when only the Scer\GAL4TrpA1-AB-G4 driver is used and non-detectable with just the Scer\GAL4TrpA1-CD-G4.

Rh6+t2.6 rescues the auditory response defects (rescues both mechanical amplification and electrical response) seen in Rh61 mutants.

Images (0)
Stocks (4)
Notes on Origin

Present in the y1; cn1, bw1, sp1 strain, Bloomington stock number 2057, used for obtaining the whole genome sequence.


Mutation found during genome annotation of the strain used in the genome sequencing project.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (27)