FB2025_05 , released December 11, 2025
Allele: Dmel\NmnatWR.UAS.PD
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General Information
Symbol
Dmel\NmnatWR.UAS.PD
Species
D. melanogaster
Name
FlyBase ID
FBal0198137
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Carried in construct
Cytology
Description

UASt regulatory sequences drive expression of the AT23490 cDNA, in which two key residues required for substrate binding have been mutated (amino acid substitutions W98G and R224A). This results in an enzymatically inactive form of Nmnat.

Allele components
Component
Use(s)
Encoded product / tool
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 ( 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

Expression of NmnatWR.Scer\UAS under the control of Scer\GAL4elav.PU has no effect on learning and memory in an aversive phototaxis assay at 20 days post eclosion. No locomotor activity are seen, as measured by climbing performance and brains do not display any morphological defects.

Expression of NmnatWR.Scer\UAS under the control of Scer\GAL4GMR.PF protects flies against neuronal degeneration in response to intense light exposure; eyes expressing this transgene show less vacuolization and a higher number of rhabdomeres than wild-type flies in response to 30 days of light exposure.

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

Expression of 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.

Co-expression of NmnatWR.Scer\UAS suppresses the rhabdomere degeneration phenotype induced by Scer\GAL4GMR.PF>Atx-1Scer\UAS.cTa.

The loss of rhabdomere phenotype of rdgAunspecified mutants is significantly rescued by either NmnatScer\UAS.cZa or NmnatWR.Scer\UAS, under the control of Scer\GAL4GMR.PF. The size of vacuoles that are present in the retina and photoreceptors of rdgAunspecified mutants are reduced by expression of NmnatWR.Scer\UAS, but not NmnatScer\UAS.cZa.

The number of rhabdomeres per ommatidium is significantly rescued in trpP365 flies by expression of either NmnatScer\UAS.cZa or NmnatWR.Scer\UAS under the control of Scer\GAL4GMR.PF. However, the vacuolarization that occurs in trpP365 retinae and photoreceptors is not suppressed by either transgene.

Xenogenetic Interactions
Statement
Reference

Expression of NmnatWR.Scer\UAS suppresses the learning and memory deficits seen in 20 day old flies expressing Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4elav.PU. The climbing defects are partially suppressed. The climbing defects are also suppressed. The brain vacuolisation seen at 20 days post eclosion is almost completely suppressed.

Expression of NmnatWR.Scer\UAS suppresses the learning and memory deficits seen in 20 day old flies expressing Hsap\MAPTR406W.Scer\UAS under the control of Scer\GAL4elav.PU. The climbing defects are also suppressed. The brain vacuolisation seen at 20 days post eclosion is almost completely suppressed and fewer apoptotic cells are seen in the midbrain.

The rough eye and rhabdomere phenotypes of Scer\GAL4GMR.PF>Hsap\ATXN182Q.Scer\UAS are partially suppressed by co-expression of NmnatWR.Scer\UAS.

Complementation and Rescue Data
Fails to rescue
Comments

Post-synaptic expression of the enzymatically-inactive NmnatWR.Scer\UAS transgene, under the control of Scer\GAL421-7 is sufficient to rescue the dendritic phenotypes observed in NmnatΔ4790-2 ddaC clones, demonstrating a cell-autonomous function for Nmnat in the proper maintenance of class IV dendrites.

Expression of NmnatWR.Scer\UAS in Nmnat1 mutant photoreceptors, driven by Scer\GAL4GMR.PF, fully rescues synaptic structures and mostly restores rhabdomere size. However, expression of this transgene in Nmnat1 whole organisms, driven by Scer\GAL4Act5C.PI, fails to rescue the lethality.

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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
NmnatWR.Scer\UAS
NmnatWR.UAS.PD
NmnatWR.UAS
Name Synonyms
Secondary FlyBase IDs
    References (6)