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General Information
Symbol
Dmel\drke0A
Species
D. melanogaster
Name
FlyBase ID
FBal0287941
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
drkeOA
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C13497514T

Amino acid change:

H106Y | drk-PA; H106Y | drk-PB; H106Y | drk-PC; H106Y | drk-PD; H106Y | drk-PF

Reported amino acid change:

H106Y

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: H106Y.

Amino acid replacement: H106Y. H106 is a highly conserved residue among SH2 domains.

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 ( 0 )
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

drk6/drke0A transheterozygotes exhibit disorganized scolopidia (as revealed by phalloidin staining, which labels cap rods, scolopale rods, and the actin bundles within the cilia of the mechanosensory neurons).

Olfactory association learning is lower in drke0A heterozygotes compared to controls.

Histological and immunohistochemical examination of drke0A heterozygous heads with multiple antigenic markers does not reveal and gross structural anomalies in the brain. Avoidance of odors used as CS and electroshock (US) are no different from that of controls. Heterozygous mutants exhibit normal odor avoidance after pre-exposure to electric shock.

Mutation disrupts development of receptor cell R7.

Reduces the ability of a cell to develop as an R7 cell or as any other photoreceptor.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Enhancer of
Statement
Reference

drk[+], drke0A, drke0A is an enhancer of abnormal size | adult stage phenotype of sl2

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

drk[+], drke0A, drke0A is a suppressor of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

drk[+], drke0A, drke0A is a suppressor of visible phenotype of Src64BΔ540.hs.sev

NOT Suppressor of
Phenotype Manifest In
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

drk[+], drke0A, drke0A is a suppressor | partially of wing vein | ectopic phenotype of sl2

drk[+], drke0A, drke0A is a suppressor of dorsal appendage phenotype of CblL.UAS, Scer\GAL4EQ1

drk[+], drke0A, drke0A is a suppressor of dorsal appendage phenotype of CblL.Δ70Z.UAS, Scer\GAL4EQ1

drk[+], drke0A, drke0A is a suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

drk[+], drke0A, drke0A is a suppressor of eye phenotype of Src64BΔ540.hs.sev

drke0A/drke0A is a suppressor of phenotype of Src42AKR.hs.2sev

drkE(sev)2B/drke0A is a suppressor of phenotype of svp1.sev

drkE(sev)2B/drke0A is a suppressor of phenotype of svp2.sev

drke0A/drke0A is a suppressor of phenotype of svp2.sev

drkE(sev)2B/drke0A is a suppressor of phenotype of tor11D

NOT Suppressor of
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

dock04723 drke0A double mutant embryos do not show defects in myoblast fusion.

One copy of drke0A enhances the reduction in wing blade area seen in homozygous sl2 males.

One copy of drke0A does not enhance the reduction in wing blade area seen in homozygous sl9 males.

One copy of drke0A partially suppresses the ectopic wing vein phenotype seen in sl2 homozygotes.

One copy of drke0A partially suppresses the percentage of sl2 mutant ommatidia that contain extra R7 photoreceptors.

drke0A/+ significantly suppresses the ventralised egg shell phenotype observed when CblL.Scer\UAS is expressed in follicle cells under the control of Scer\GAL4EQ1.

drke0A/+ fails to suppresses the ventralised egg shell phenotype observed when CblL.mPR.Scer\UAS is expressed in follicle cells under the control of Scer\GAL4EQ1.

The dorsalised eggshell phenotype observed when CblL.Δ70Z.Scer\UAS is expressed under the control of Scer\GAL4EQ1 is suppressed in a drke0A/+ background.

Expression of phlfl.Scer\UAS under the control of Scer\GAL4c747 results in full reversal of the learning deficit of drke0A heterozygotes.

Expression of phlScer\UAS.F179 under the control of Scer\GAL4c747 results in full reversal of the learning deficit of drke0A heterozygotes.

The presence of a drke0A background does not affect ectopic wing vein formation in cswY279C.Scer\UAS (Scer\GAL4tub) mutants.

drke0A/+ suppresses the ectopic wing vein phenotype caused by expression of Pi3K68DKD.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL469B.

Weakly enhances the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).

Has no effect on the eye phenotype caused by C3GScer\UAS.T:Hsap\MYC,T:Ggal\Myr3 expressed under the control of Scer\GAL4GMR.PF. Has no effect on the wing vein phenotype caused by C3GScer\UAS.T:Hsap\MYC,T:Ggal\Myr3 expressed under the control of Scer\GAL4dpp.blk1.

drke0A significantly suppresses the formation of extra outer photoreceptors caused by B-H1sev.PH, although it does not affect the loss of R7 cell phenotype caused by B-H1sev.PH.

Presence of the mutation in Src64BΔ540.hs.sev flies alleviates the rough eye phenotype.

No effect on the faf eye phenotype.

Suppressor of the dosage-dependent (two or more copies of P{sev-svp1} or P{sev-svp2}) transformation of cone cells into R7 photoreceptors and at a lower frequency R7 cells into outer photoreceptors.

Mutation has no effect on the rough eye phenotype caused by two insertions of P{GMR-Rho1}.

Suppression of the rough eye phenotype (formation of extra R7 cells) caused by P{sev-svp2} and enhancement of the P{ro-svp1} rough eye phenotype (loss of one or more outer photoreceptors from many of the ommatidia).

Weak suppressor of tor11D phenotype, embryos display 2 to 3 abdominal denticle belts.

In drkE(sev)2B sevB4 combination adults nearly all of the ommatidia lack the R7 cell. The presence of P{sev-drk} restores an R7 cell to most ommatidia. Homozygous drkE(sev)2B clones in P{sevRas1.V12} flies frequently develop as photoreceptors despite the lack of drk function. The rescued cells can be inner R1-R6-like photoreceptors or outer R7-like photoreceptors.

Enhances the sevB4 phenotype: disrupts sevB4 protein signalling.

Xenogenetic Interactions
Statement
Reference

The penetrance of the Fas2-positive axon crossover phenotype seen in embryos carrying Khc::Ggal\MLCKKA.ftz is increased if they are also homozygous for drke0A.

Complementation and Rescue Data
Rescued by
Comments

The lethality seen in drkR1/drkE(sev)2B transheterozygotes can be rescued by drk product supplied under a heat shock promoter.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

The recessive lethal mutation, "l(2)E(sev)2B", is the same lesion as drkE(sev)2B.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (29)