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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

Duplication at the CycG locus, with a frame-shift mutation in each copy of the gene. The distal gene copy carries an additional deletion distal to the BamHI site of approximately 350bp. A w+mW.hs marker has been inserted between the two copies as part of the targeting event.

Insertion components
Caused by aberration
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 ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Disease-implicated variant(s)
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

CycGHR7 heterozygous females lay eggs with normal dorsal appendages when compared to controls.

CycGHR7/CycGHR7 larvae have a similar phenotype to starved wild-type controls, even though fed: high fat content, with aggregations of large lipid droplets in the fat body and oenocytes, and signs of autophagy in the fat body.

CycGHR7/CycGHR7 mutants do not show abnormal wing phenotypes.

CycGHR7 females lay significantly fewer eggs per day than controls.

CycGHR7 homozygous mutants are developmentally delayed, smaller and lighter than wild-type controls but their food ingestion at larval stage is normal.

The number and size of cells in the adult wings of CycGHR7 homozygotes is reduced compared to wild-type.

Clones of cells homozygous mutant for CycGHR7 are smaller than their wild-type twinspot counterparts in both eye-antennal and wing discs.

CycGHR7 homozygotes have decreased lifespan upon wet starvation compared to wild-type controls.

CycGHR7 homozygote larvae are lighter and accumulate more fat than wild-type controls. The fat body of CycGHR7 homozygote larvae shows an aggregation of lipid droplets, similar to starved wild-type larvae, even when fed.

Oenocytes of the CycGHR7/CycGHR7 larvae accumulate lipid droplets regardless of their fed/starved status.

The salivary glands of CycGHR7 mutant larvae are smaller than in wild-type controls and have smaller nuclei.

CycGeoC/CycGHR7 transheterozygotes show developmental delay, reduced body size and weight, higher fat content and decreased egg laying rate.

Homozygous females are sterile and produce ventralised eggs that have fused dorsal appendages. Eggs derived from homozygous female germline clones develop eggs with a similar phenotype.

Mutant oocytes show defects in karyosome morphology: the DNA is attached to the oocyte nuclear membrane instead of being localised to the centre of the nucleus in 53% of egg chambers.

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

CycGHR7/CycGHR7 is an enhancer of visible phenotype of net1

CycGHR7 is an enhancer of visible phenotype of rhove-1

CycGHR7/CycGHR7 is an enhancer of visible | dominant phenotype of DlB2

CycGHR7/CycGHR7 is an enhancer of visible | dominant phenotype of HP8

Suppressor of

CycGHR7 is a suppressor of visible phenotype of vn1

Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
Suppressor of

CycGHR7 is a suppressor of wing vein | adult stage phenotype of vn1

Additional Comments
Genetic Interactions

Xrcc2CC homozygous females in the heterozygous background of CycGHR7 lay eggs with defective dorsal appendages (fused, narrowly spaced, branched or shortened) when compared to controls.

The penetrance of the wing notching phenotype in CycGHR7/+;Df(1)N-54l9/+ double heterozygote adult flies is about the same as in the Df(1)N-54l9/+ single heterozygote but is decreased in CycGHR7/CycGHR7;Df(1)N-54l9/+ flies.

CycGeoC/+;Df(1)N-54l9/+ adult flies show significant L3 vein thickening compared to either CycGHR7/CycGHR7;Df(1)N-54l9/+ or CycGHR7 mutant alone.

The vein knotting phenotype seen in N+tCos479/+;CycGHR7/+ mutants is enhanced in N+tCos479/+;CycGHR7/CycGHR7 flies, more so in males than in females.

Su(H)del47/+;CycGHR7/CycGHR7 display no phenotypic defects in adult wings.

The vein thickening phenotype of DlB2 heterozygotes is enhanced by combination with CycGHR7. The severity of the phenotype differs with gender and vein position.

Proportion of flies with both L4 and L5 vein shortening phenotype was significantly increased in HP8/+,CycGHR7/CycGHR7 mutants compared to HP8/+ alone.

rhove-1,vn1 double mutants almost completely lack veins in the adult wing. This phenotype was not changed by a further loss of CyG function in rhove-1,vn1,CycGHR7 triple mutants.

The vein loss phenotype of rhove-1 is slightly enhanced in rhove-1,CycGHR7 double mutants but the effect is limited to L4 vein.

The loss of vein material in vn1 is mildly suppressed in vn1,CycGHR7 double mutants.

The net1 phenotype (ectopic veins, vein networking) can be enhanced by combination with CycGHR7 but also by combination with mutant alleles of unrelated factors ru1 or sp1 demonstrating high susceptibility of the net1 phenotype to perturbed genetic background.

The reduced body size and weight of CycGHR7 homozygote adults is fully rescued by combination with wdb mutant alleles in a heteroallelic state: the CycGHR7,wdbdw/CycGHR7,wdb14 flies have normal both body size and weight.

The reduced body weight of CycGHR7 larvae is fully rescued by ectopic expression of Akt1Scer\UAS.Exel driven by Scer\GAL4Lsp2.PH.

The lipid droplet accumulation in oenocytes of CycGHR7 mutant larvae is highly suppressed by ectopic expression of Akt1Scer\UAS.Exel under the control of the Scer\GAL4Lsp2.PH driver.

The ventralised eggshell phenotype seen in eggs derived from homozygous CycGHR7 females is suppressed in more than 90% of eggs if the females are also carrying either mei-W681/mei-W68k05603, lokp6/Df(2L)BSC258 or mei-41RT1/Df(1)BSC772.

The ventralised eggshell phenotype seen in eggs derived from homozygous CycGHR7 females is partially suppressed by Df(2L)BSC258/+.

The ventralised eggshell phenotype of eggs derived from spn-BBU CycGHR7/spn-B2 CycGHR7 double mutant females is enhanced compared to the defects seen in eggs from spn-BBU/spn-B2 and CycGHR7/CycGHR7 single mutant females.

Eggs derived from Brca256E/Brca2KO ; CycGHR7/CycGHR7 double mutant females have a mild eggshell patterning defect, which is not altered compared to the defect seen in eggs derived from Brca256E/Brca2KO single mutant females.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

The reduced body weight of CycGHR7 homozygote adults can be ameliorated by ubiquitous ectopic expression of CycGScer\UAS.P\T.cNa under the Scer\GAL4da.PU driver, even though CycGScer\UAS.P\T.cNa;Scer\GAL4da.PU expression in a wild-type CycG background results in flies that are themselves slimmer than wild-type controls.

The reduced body weight of CycGHR7 homozygote adults and larvae is fully reversed by expression of CycGhs.PF even at ambient temperature.

The reduced egg laying rate of CycGHR7 females can be fully rescued by ectopic expression of CycGhs.PF at ambient temperature.

Expression of CycGScer\UAS.P\T.cNa under the control of Scer\GAL4da.G32 almost completely rescues the eggshell patterning defects of eggs derived from homozygous CycGHR7 females.

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Synonyms and Secondary IDs (3)
Reported As
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Secondary FlyBase IDs
    References (5)