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General Information
Symbol
Dmel\Ephx652
Species
D. melanogaster
Name
FlyBase ID
FBal0196836
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of the P{hsp26-pt-T} element that results in deletion of the first three exons of Eph (up to amino acid residue 79 of the expressed protein) and 5' sequences of the onecut gene (up to 368bp from its translation start site).

Caused by aberration
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

Mutant larvae fail to encapsulate eggs when parasitised by the avirulent L. boulardi wasp strain G486 (no melanisation is seen). Plasmatocytes fully cover the egg, while lamellocytes partially cover it.

The Ephx652 mutation has only a minor effect on baseline synaptic transmission at the neuromuscular junction (NMJ).

Ephx652 flies have no obvious morphological defects.

Ephx652 embryos show no obvious defect in overall axon tract organization.

Ephx652 mutants show defects in the formation of the dorsal lobe of the mushroom body throughout development. Both Ephx652 embryos and pupae show reduced dorsal projections. In 60% of Ephx652 third instar larvae, the dorsal lobe projections of the γ neurons are either reduced compared to wild type or missing. Reduced dorsal lobe projections are accompanied by increased medial axonal projections. In 60% of adults, the α' and α lobes are reduced or absent and the β' and β lobes show an increase in thickness. In 10% of cases the β lobes appear to be fused at the midline.

Analysis of individual Ephx652 α/β neuron clones within the mushroom body shows that these neurons bifurcate normally, but sometimes extend both branches into the β lobe, instead of extending one branch dorsally along the α lobe. When this defect occurs, supernumerary branches can be seen along the length of the β lobe. The extent to which the neuron projections are defective reflects the overall severity of the mushroom body phenotype; in Ephx652 mushroom bodies where the α lobe is missing, all neurons in a clone show projection defects, while in mushroom bodies with a normal overall morphology, α/β neuron clones show normal bifurcation and branching.

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

The neuromuscular junction (NMJ) bouton numbers in GluRIIASP16; ;Ephx652 double mutants are not significantly different from that of the GluRIIASP16 single mutant.

The spontaneous miniature release event (mepsp) amplitudes are significantly decreased in GluRIIASP16; ;Ephx652 double mutants compared to Ephx652 single mutants or wild-type. This double mutant phenotype is similar to the one observed in GluRIIASP16 single mutants.

The average homeostatic increase in presynaptic release observed in GluRIIASP16 single mutants is significantly suppressed in GluRIIASP16; ;Ephx652 double mutants.

The heterozygous Ephx652/+ mutation alone does not significantly change the recessive GluRIIASP16 phenotype involving the synaptic homeostatic compensation at the neuromuscular junction (NMJ).

The combination of ExnEY01953/+ and Ephx652/+ heterozygous mutations 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).

Expression of EphrinScer\UAS.T:Hsap\MYC in the midline glia of embryos, driven by Scer\GAL4sim.PS, in an Ephx652 background does not cause the disruption of commissural axons seen when the transgene is expressed in wild-type embryos.

Ephx652/onecutx122 and Ephx652/onecutx49 mutants show no defects in dorsal lobe formation, indicating that the dorsal lobe phenotype of Ephx652 mutants is due to the disruption of Eph.

Flies that express EphrinScer\UAS.T:Hsap\MYC under the control of either Scer\GAL4OK107 or Scer\GAL4elav.PLu, in an Ephx652 background, show the same α'/α lobe defects as flies expressing the transgene in a wild-type background and as Ephx652 flies with no transgene.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (4)