FB2025_01 , released February 20, 2025
Allele: Dmel\wnd1
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General Information
Symbol
Dmel\wnd1
Species
D. melanogaster
Name
FlyBase ID
FBal0194609
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

wnd1 habours a mutation in a conserved residue in the kinase domain.

Amino acid replacement: G172E.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G19629385A

Amino acid change:

G173E | wnd-PA; G173E | wnd-PB; G173E | wnd-PC; G146E | wnd-PD

Reported amino acid change:

G172E

Comment:

The mutation was mapped to G173 because there is no G at position 172 in the reference sequence. Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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
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/wnd3 transheterozygotes do not show grooming defects, nor any obvious adult mushroom body defects.

wnd1/wnd3 animals show severely reduced axon outgrowth in ddaC neurons after axon severing, while dendrite regeneration after complete removal of the dendrites appears normal.

wnd1/Df(3L)ED229 larvae show defects in axonal transport, resulting in accumulations of protein in nerves.

wnd1/wnd2 and wnd1/Df(3L)ED229 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.

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.

wnd1 mutants exhibit wild-type synapse size.

wnd1 mutants show no reduction in synaptic growth.

wnd1/wnd2 mutants exhibit normal synaptic function.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference
Phenotype Manifest In
Suppressor of
Statement
Reference

wnd[+]/wnd1 is a suppressor of synapse phenotype of Scer\GAL4elav-C155, sggA81T.UAS

wnd[+]/wnd1 is a suppressor of neuromuscular junction phenotype of hiwND8

wnd[+]/wnd1 is a suppressor of bouton phenotype of hiwND8

wnd1/wnd2 is a suppressor of bouton phenotype of hiwND8

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.

A wnd1 heterozygous background partially suppresses the high levels of autophagy and bouton number found upon expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.PLu. A wnd1 homozygous background completely suppresses the neuromuscular junction overgrowth phenotype.

A wnd1/+ background completely abolishes the synapse growth seen through sggA81T.Scer\UAS expression pan-neuronally under the control of Scer\GAL4elav-C155.

Removing one copy of wnd1 suppresses the hiwND8 neuromuscular junction of muscle 4 phenotype by approximately 50%.

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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Complementation and Rescue Data
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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (15)