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General Information
Symbol
Dmel\Ank2f02001
Species
D. melanogaster
Name
FlyBase ID
FBal0181704
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ank22001
Key Links
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference
    Insertion components
    PBac{WH}Ank2f02001
    Product class / Tool use(s)
    Encoded product / tool
    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

    Ank2f02001/Ank2f02001 mutant 1st, 2nd and 3rd instar larval neuromuscular junctions exhibit abberant microtubule organization, with aggregates of central microtubules; and a significant increase in synaptic retraction frequency at later larval stages, but no defect in the presence of microtubules at terminal boutons, as compared to controls.

    Ank2f02001 mutants exhibit a significant increase in synaptic retractions compared with controls.

    Sound-evoked compound action potentials in the antennal nerve are not significantly different from wild type in mutant flies. However, nonlinear mechanical amplification is significantly reduced compared to wild type.

    Ank2f02001 mutant third instar larvae show severe NMJ degeneration, leading to complete elimination of the presynaptic nerve terminal at many NMJs. Loss of Ank2 also causes axonal blockages and severe disruption of the axonal and synaptic microtubule skeleton.

    Homozygous egrΔ25 mutants show large defects in EPSP amplitude compared to wild-type. A large number of recording are seen that have average EPSPs below 25mV.

    Neuromuscular junctions of mutant larvae have fewer but larger boutons than normal.

    Neuromuscular junctions of Ank2RM5-1/Ank2f02001 larvae have fewer but larger boutons than normal. The synaptic span (the widest extension of synaptic branches along a muscle fibre) is reduced compared to wild type.

    Homozygotes die at late larval/early pupal stages.

    Homozygotes show severe synaptic retractions at more than 60% of all neuromuscular junctions (NMJs) on muscles 6/7.

    Ank2f02001/Df(3L)RM5-2 and Ank2f02001/Ank2f00518 animals die as third instar larvae/early pupae, and they show severe synaptic retractions at the NMJs.

    The severity of the synaptic retraction phenotype that is seen at the NMJs of Ank2f02001/Df(3L)RM5-2 animals increases progressively during larval development.

    Ank2f02001/Df(3L)RM5-2 third instar larvae show defects in synaptic transmission and motoneuron excitability at the NMJ. Defects in in synapse morphology are also seen at the NMJ, with enlarged presynaptic membrane compartments. The presynaptic microtubule cytoskeleton shows abnormal organisation. Ultrastructurally, NMJs show hallmarks of synapse degeneration, including accumulations of endosomal/vacuole-like membrane profiles. In addition, giant synaptic boutons are seen at the NMJ. The boutons are elongated laterally, and multiple active zones can be detected. In addition, large vesicles are present. Large accumulations of microtubules can also be seen, with vesicles being absent from these regions.

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

    Presynaptic expression of CkIIαScer\UAS.N.T:Ivir\HA1 in Ank2f02001 homozygous mutants significantly alleviates the synaptic retraction phenotype.

    Presynaptic expression of CkIIαK66M.Scer\UAS.N.T:Ivir\HA1 in Ank2f02001 homozygous mutants enhances the synaptic retraction phenotype.

    Removal of one copy of CkIIαP1 in a Ank2f02001 homozygous background significantly increases the frequency of synaptic retractions.

    Removal of one copy of Ank2f02001 in a CkIIαP1 homozygous background significantly increases the frequency of synaptic retractions.

    egrΔ25 partially suppresses the NMJ degeneration seen in Ank2f02001 mutant third instar larvae. The axonal blockages and microtubule disruption are not suppressed.

    egrΔ25 partially suppresses the synaptic transmission defects seen in Ank2f02001 mutants. A near complete rescue in the number of small EPSPs is seen, however average EPSP amplitude is not completely restored to wild type levels.

    Expression of egrdsRNA.Scer\UAS under the control of Scer\GAL4egr-GAL4 partially suppresses the NMJ degeneration seen in Ank2f02001 mutant third instar larvae.

    Expression of wgndsRNA.Scer\UAS under the control of Scer\GAL4elav-C155 partially suppresses the NMJ degeneration seen in Ank2f02001 mutant third instar larvae. The axonal blockages and microtubule disruption are not suppressed.

    Expression of wgndsRNA.Scer\UAS under the control of Scer\GAL4elav-C155 partially suppresses the synaptic transmission defects seen in Ank2f02001 mutants. A near complete rescue in the number of small EPSPs is seen, however average EPSP amplitude is not completely restored to wild type levels.

    Homozygous Dcp-1Prev1 suppresses the NMJ degeneration seen in Ank2f02001 mutants. One copy of Dcp-1Prev1 is also able to partially suppress the phenotype.

    Homozygous dl1 does not suppress the NMJ degeneration seen in Ank2f02001 mutant larvae.

    Homozygous debclE26 partially suppresses the NMJ degeneration seen in Ank2f02001 mutants.

    Homozygous ArkCD4 partially suppresses the NMJ degeneration seen in Ank2f02001 mutants.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Images (0)
    Mutant
    Wild-type
    Stocks (1)
    Notes on Origin
    Discoverer
    Comments
    Comments

    Precise excision of the insertion reverts the neuromuscular junction phenotype.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (6)
    References (12)