FB2025_02 , released April 17, 2025
Allele: Dmel\EphDN.UAS
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General Information
Symbol
Dmel\EphDN.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0135987
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

Lacks residues 675-1035 i.e. consists of normal extracellular and transmembrane domains but lacks most of the intracellular domain including the kinase, SAM and PDZ-binding domains.

Allele components
Component
Use(s)
Encoded product / tool
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

Expression of EphDN.Scer\UAS with Scer\GAL4elav-C155 or Scer\GAL4C57 has no significant effect on spontaneous miniature release event (mepsp) amplitudes or quantal content at the neuromuscular junction (NMJ), as compared to wild-type.

When expression is driven by Scer\GAL4ey.PH severe defects are produced in the midline projections of photoreceptor and medulla cortical axon projections. Separation into dorsal and ventral fascicles at the midline of the lamina fails. The large fascicle often projects to ectopic locations. At the midline of the medulla the optic ganglion is disrupted - medulla neuropil is primarily absent and the area devoid of neurons fills with glia that would normally border the neuropil. When expression is driven by Scer\GAL4ap-md544, a visible phenotype results. Axons of midline cortical cells project abnormally, though those in dorsal and ventral positions project normally. When expression is driven in somatic cell clones in the developing eye, by Scer\GAL4αTub84B.PP, R7 and R8 axons are abnormally fasciculated when the clone is large. When the clone includes the cortex the defects map largely to the midline. Cortical cell axon projection defects are enhanced at the border between clone and non-clone tissue. Projections dorsoventral to the clone are generally wild type.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhancer of
Suppressor of
NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The rough eye phenotype of Scer\GAL4hs.2sev, EphrinScer\UAS.cDa flies is suppressed by co-expression of EphDN.Scer\UAS.

Expression of EphDN.Scer\UAS with Scer\GAL4C57 does not significantly change the GluRIIASP16 phenotype involving spontaneous miniature release event (mepsp) amplitudes or quantal content at the neuromuscular junction (NMJ).

Expression of EphDN.Scer\UAS with Scer\GAL4elav-C155 does not significantly change the GluRIIASP16 phenotype involving spontaneous miniature release event (mepsp) amplitudes, while it does partially suppress the GluRIIASP16 quantal content phenotype at the neuromuscular junction (NMJ).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
EphDN.Scer\UAS
EphDN.UAS
Name Synonyms
Secondary FlyBase IDs
    References (3)