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General Information
Symbol
Dmel\axed2094
Species
D. melanogaster
Name
FlyBase ID
FBal0327536
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
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

May be a regulatory mutation, as a molecular lesion within the axed ORF could not be identified.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Flies carrying axed2094 mutant somatic clones show defective injury-induced axon degeneration: severed axons (either in sensory neurons in the wing or in cholinergic olfactory receptor neurons) remain intact for a full week after an axotomy (or even 50 days in the latter case), instead of being cleared away. After axotomy of mechanosensory neurons in the Johnston's organ, the persisting severed axons can still elicit grooming behavior upon optogenetic stimulation of the neurons.

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

axed2094 is a non-suppressor of eye phenotype of hidGMR.PG

Additional Comments
Genetic Interactions
Statement
Reference

MARCM clones in sensory neurons in the adult wing expressing Ect4ΔARM.Scer\UAS.T:Hsap\MYC driven by Scer\GAL4VGlut-OK371 undergo spontaneous cell body and axon degeneration which can be suppressed by combination with axed2094.

The axon and cell body degeneration in sensory neuron clones in the adult wing mutant for NmnatΔ4790-1 or expressing NmnatGD8082 under the control of Scer\GAL4VGlut-OK371 can be fully rescued by combination with axed2094 or by axed2094 and Ect4896 together.

The NmnatΔ4790-1,axed2094 double mutant clones display defective injury-induced axon degeneration (severed axons remain intact following an axotomy, instead of being cleared away) which cannot be overcome by expressing Ect4ΔARM.Scer\UAS.T:Hsap\MYC under the Scer\GAL4VGlut-OK371 driver in the mutant clones.

The small eye phenotype resulting from the cell death induced by expression of hidGMR.PG is not suppressed by combination with axed2094.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Comments

The defective injury-induced axon degeneration observed in flies carrying axed2094 mutant neural clones (severed axons in sensory neurons in the adult wing remain intact following an axotomy, instead of being cleared away) can be rescued by clonal Scer\GAL4VGlut-OK371-driven expression of any of the following: axedScer\UAS.long, axedΔBTB.Scer\UAS, axedΔBACK.Scer\UAS or axedΔCterm.Scer\UAS.

Any of the following: axed0011, axedCrisprA, axedCrisprB, axedCrisprC, axedEx07, axedEx65 or axedEx96 fails to complement the lethality of axed2094 mutants, while Ect4896 fails to do so.

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
Name Synonyms
Secondary FlyBase IDs
    References (1)