FB2025_01 , released February 20, 2025
Allele: Dmel\NmnatΔ4790-1
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General Information
Symbol
Dmel\NmnatΔ4790-1
Species
D. melanogaster
Name
FlyBase ID
FBal0198134
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

Imprecise excision of the P{EPgy2} element, resulting in deletion of the first four exons of the Nmnat gene.

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

NmnatΔ4790-1 mutant clones in sensory neurons in the adult wing undergo rapid degeneration affecting cell bodies as well as axons.

Flies with eyes that contain NmnatΔ4790-1 clones show reduced depolarization and on/off responses in electroretinogram (ERG) recordings and show photoreceptor synaptic defects.

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

The axon and cell body degeneration in NmnatΔ4790-1 sensory neuron clones in the adult wing can be fully rescued by combination with axed0011, axed2094 or by axed2094 and Ect4896 together, but not by combination with either Ect4896 or Ect44621 alone.

The NmnatΔ4790-1,axed0011 as well as 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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)