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General Information
Symbol
Dmel\Sarm896
Species
D. melanogaster
Name
FlyBase ID
FBal0277677
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dsarm896
Key Links
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Nucleotide change:

    C8103298T

    Amino acid change:

    Q603term | Ect4-PD; Q326term | Ect4-PE; Q352term | Ect4-PF; Q528term | Ect4-PG; Q352term | Ect4-PH; Q696term | Ect4-PI; Q352term | Ect4-PJ; Q696term | Ect4-PK

    Reported amino acid change:

    Q603term

    Comment:

    Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    Amino acid replacement: Q603term.

    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

    Flies carrying Ect4896 mutant somatic clones show defective injury-induced axon degeneration (severed sensory neuron axons in the adult wing remain intact for a full week after an axotomy, instead of being cleared away by day 5). After axotomy of mechanosensory neurons in the Johnston's organ, the persisting severed axons can still elicit grooming behavior upon optogenetic stimulation of the neurons.

    Ect4896 has a strong protective effect on L1 vein neurons following axotomy. Whereas wild type axons undergo fragmentation, many severed but intact axons are observed.

    The axons of homozygous olfactory receptor neurons remain intact 1 week after axon severing (in contrast to wild type). The mutant axons remain fully intact 30 days after axon severing, and a significant but reduced number remain intact 50 days after axon severing.

    Pruning of axons and dendrites during metamorphosis occurs normally in homozygous mushroom body gamma neuron clones.

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

    Ect4896 mutant MARCM clones in sensory neurons in the adult wing expressing Ect4ΔARM.Scer\UAS.T:Hsap\MYC driven by Scer\GAL4VGlut-OK371 undergo spontaneous cell body and axon degeneration.

    The axon and cell body degeneration in sensory neuron clones in the adult wing mutant for NmnatΔ4790-1 or expressing NmnatGD8082 under the control of Scer\GAL4VGlut-OK371 can be fully rescued by combination with axed2094 and Ect4896 together, but not - or only weakly - by combination with Ect4896 alone.

    Ect4896 does not suppress the degeneration seen in leg motor neuron clones expressing Hsap\TARDBPQ331K.Scer\UAS.cSa under the control of Scer\GAL4VGlut-OK371.

    Homozygous Ect4896 clones fail to suppress the cell death in the eye caused by WGMR.PG.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Partially rescued by
    Comments

    Ect4896 complements the lethality of either axed2094 or axed0011 mutants.

    The axon death defect (severed sensory neuron axons in the adult wing persist after an axotomy, instead of being cleared away) observed in flies carrying Ect4896 neuronal mutant clones can be rescued by combination with Ect4+tOa or by Scer\GAL4VGlut-OK371-driven expression of either Ect4ΔARM.ΔTIR.Scer\UAS.T:Ivir\HA1, and partially rescued by expression of Ect4Scer\UAS.cOa or Ect4Scer\UAS.T:Avic\GFP-EGFP but cannot be rescued by expression of any of the following: Ect4ΔSAM.Scer\UAS.T:Avic\GFP-EGFP, Ect4ΔTIR.Scer\UAS.T:Avic\GFP-EGFP, Ect4ΔARM.ΔSAM.Scer\UAS.T:Avic\GFP-EGFP or Ect4ΔSAM.ΔTIR.Scer\UAS.T:Avic\GFP-EGFP in the mutant clones.

    Expression of Ect4Scer\UAS.cOa under the control of Scer\GAL4Or22a.7.717 reverts the suppression of axonal degeneration after axon severing which is seen in Ect4896 mutant neurons.

    Ect4+tOa rescues the lethality and reverts the suppression of axonal degeneration after axon severing which is seen in Ect4896/Df(3L)BSC795 and Ect4896/Ect44621 animals.

    Images (0)
    Mutant
    Wild-type
    Stocks (0)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (5)
    Reported As
    Name Synonyms
    Secondary FlyBase IDs
      References (6)