FB2024_03 , released June 25, 2024
Allele: Dmel\wnd2
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General Information
Symbol
Dmel\wnd2
Species
D. melanogaster
Name
FlyBase ID
FBal0194610
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Amino acid replacement: term978N.

Mutation in the wild-type stop codon that adds an extra 104 residues to the protein.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Reported amino acid change:

term978N

Comment:

The reported stop to Asn amino acid change (TAA to AAT/C) requires substitution at two positions in the codon.

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 ( 1 )
Disease
Interaction
References
ameliorates  tauopathy
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

wnd1/wnd2 larvae show an increase in maximum bouton diameter at the neuromuscular junction compared to controls.

The ability of injured axons to sprout after injury is inhibited in wnd1/wnd2 larvae.

Under control conditions, wnd2/wnd3 transheterozygous third instar larvae do not display significant changes in the number of sensory axons per nerve, as compared to controls.

Axonal sprouting of the injured axon after a crush injury to the segmental nerve in third instar larvae is dramatically inhibited in wnd1/wnd2 animals.

wnd2 mutants exhibit wild-type synapse size.

wnd1/wnd2 mutants exhibit normal synaptic function.

External Data
Interactions
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Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

The synaptic overgrowth phenotype (increase in bouton number) seen at the neuromuscular junction in larvae derived from homozygous SkpAGD65 females is significantly (but not completely) suppressed by wnd1/wnd2.

wnd2/+ partially suppresses the increase in bouton number seen at the neuromuscular junction in shot3/shotVV third instar larvae.

wnd2/wnd3 fully suppresses the increase in bouton number seen at the neuromuscular junction in shot3/shotVV third instar larvae.

A wnd2/+ background completely abolishes the synapse growth seen through sggA81T.Scer\UAS expression pan-neuronally under the control of Scer\GAL4elav-C155.

hiwND8; wnd1/wnd2 mutants are not significantly different from wild-type, indicating complete suppression of hiwND8.

wnd1/wnd2 mutants do not suppress the hiwND8 defect in quantal size: both the amplitude and the frequency of spontaneous miniature events in the hiwND8; wnd1/wnd2 double mutant are similar to wild-type. In contrast, the evoked potentials of the double mutant are only modestly increased, and this is due entirely to the increased quantal size. The quantal content, calculated as the excitatory junction potential (EJP) amplitude divided by the miniature EJP (mEJP) remains the same between hiwND8 and hiwND8; wnd1/wnd2 double mutants. Therefore wnd does not suppress the primary defect in hiwND8 synaptic function, the reduced number of vesicles released by the nerve.

Xenogenetic Interactions
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Reference
Complementation and Rescue Data
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Mutant
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Stocks (0)
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (12)