FB2025_01 , released February 20, 2025
Allele: Dmel\EG28EG28
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General Information
Symbol
Dmel\EG28EG28
Species
D. melanogaster
Name
FlyBase ID
FBal0244438
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 ( 0 )
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
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference

EG28EG28/EG28[+] is an enhancer of visible phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF

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

EG28EG28/EG28[+] is an enhancer of eye phenotype of DCTN1-p150Δ.UAS, Scer\GAL4GMR.PF

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

EG28EG28 dominantly enhances the eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF.

20% of giant fiber axons fail to exit the brain in adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 in a EG28EG28/+ background.

Only 3% of giant fiber axons in Gl1/+ ; EG28EG28/+ double heterozygotes lack the characteristic terminal bend, but the axons often show ectopic branching.

The electrophysiological defects seen in the giant fiber system of Gl1/+ adults are enhanced if they are also heterozygous for EG28EG28; the response latencies are significantly increased and the double heterozygous flies show poor following.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

It has not been determined whether the lethality of the chromosome is caused by the mutation that modifies the eye phenotype caused by expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF, so it is possible that the recessive lethality of the chromosome is due to a second-site mutation.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
EG28EG28
Name Synonyms
Secondary FlyBase IDs
    References (1)