FB2025_01 , released February 20, 2025
Allele: Dmel\milt33-853
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General Information
Symbol
Dmel\milt33-853
Species
D. melanogaster
Name
FlyBase ID
FBal0284439
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description
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

Mutants show loss of anterograde mitochondria transport in motor neurons.

Homozygous olfactory receptor neuron (ORN) clones result in loss of ORN cell bodies and axons. Defects in the organisation of the antennal lobe neuropil, including loss of glomeruli is seen.

Homozygous single cell motor neuron clones in larvae show normal development and axon and synaptic morphology, but show loss of anterograde mitochondria transport.

Wallerian degeneration in an axotomized motor neuron within a crushed, but still continuous segmental nerve follows a similar time course in wild-type and milt33-853 motor neuron clones, with continuity being maintained at 4 hours and a heterogeneous population of continuous and fragmented axons appearing 8 hours after crushing. A significantly smaller fraction of milt33-853 axons are fragmented at 8 hours after crushing compared to wild-type axons, although all mutant and wild-type axons are fragmented by 16 hours after crushing.

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

The anterograde mitochondria transport defects of single cell milt33-853 larval motor neuron clones are not rescued by expression of NmnatScer\UAS.cZa under the control of Scer\GAL4D42.

Expression of either NmnatScer\UAS.cZa or NmnatWR.Scer\UAS under the control of Scer\GAL4elav-C155 protects both wild-type and milt33-853 motor neuron clones from degeneration after axotomy at 16 hours after crushing.

Xenogenetic Interactions
Statement
Reference

The loss of olfactory receptor neuron (ORN) cell bodies and axons and the morphological defects in the antennal lobe neuropil which are seen when homozygous milt33-853 ORN clones are induced is not suppressed by expression of Mmus\wldS.Scer\UAS under the control of Scer\GAL4Or22a.7.717.

Expression of Mmus\wldS.Scer\UAS under the control of Scer\GAL4elav-C155 protects both wild-type and milt33-853 motor neuron clones from degeneration after axotomy at 16 hours after crushing and delays Wallerian degeneration in both wild-type and milt33-853 motor neuron clones 24 hours after crushing.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
milt33-853
milton33-853
Name Synonyms
Secondary FlyBase IDs
    References (1)