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General Information
Symbol
Dmel\Dscam118
Species
D. melanogaster
Name
FlyBase ID
FBal0134278
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Dscam18
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
    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 ( 1 )
    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

    Single C4 da neurons homozygous for Dscam118, exhibit markedly reduced presynaptic arbor growth.

    Dscam118/Dscam118 late pupal MB neuron clones exhibit abnormal additional axon branches and failure in the segregation of sister branches.

    Adult single-cell Dscam18 clones of DL-1 PNs exhibit reduced dendritic elaboration in the DL-1 glomeruli and reduced axon arborization in the mushroom body calyces and lateral horns.

    Single cell clones of mushroom body α/β neurons that are homozygous for Dscam18 show axon branching defects, such as lack of segregation of sister branches (35%) and generation of additional branches at the bifurcation points (42%).

    When homozygous somatic clones are made in the mushroom body neuroblasts, normal looking γ lobes are seen, but the α/β lobes are abnormal. Being much thicker and denser than in wild-type clones, the core α/β lobes seem to be composed of many more axons. But unlike wild-type α/β axons, most mutant core α/β processes appear to fail to reach the ends of the lobes. Because no change in the number of cell bodies can be detected, the morphological changes observed in mutant bundles imply that individual α/β axons acquire supernumerary but short-ending branches in mutant clones. In addition, dramatic changes in the configuration of the α/β lobes are observed in 38% of mutant neuroblast clones. Instead of bifurcating axons at a right angle, these mutant clones project all of their α/β axons only in one direction, either dorsal or medially. These processes can exist as two distinct bundles running side by side, or can be fasciculated into a single bundle. In about 20% of clones, differences in the thickness of then axon bundles exist between the dorsal and medial fascicles. These clones also have a non cell-autonomous effect on axon guidance: When the mutant core α/β lobes extend as two distinct bundles side by side, all the wild-type α/β axons are seen to project in the same direction as mutant ones. Consistent abnormalities are observed in the projections of both α/β and α'/β' axons. If clones are induced around mid 3rd instar stage, changes in the α/β lobe configuration are found when mutant clones contain γ axons. If clones are induced after initiation of α'/β' neuron production, normal organisation of α/β lobes is observed despite uneven segregation of axonal branches. When single cell clones are made in the γ neuron, they are indistinguishable from wild-type. However mutant α'/β' and α/β axons develop abnormalities in the axon branching and projecting patterns. Axons often give rise to supernumerary branches which branch towards the termini of Mushroom body clones. In addition, these extra branches still acquire their cell type-specific morphological features, and mutant α/β axons are never incorporated into the α', β' or γ lobes. Individual neurons sometimes fail to send processes into both dorsal and medial lobes. All mutant α/β axons, when examined as isolated single axons in neuroblast clones yield multiple branches that extend randomly into the accessible lobes. Each individual axon frequently sens most or all of their supernumerary branches into only one of the lobes. In addition the multifurcation of mutant axons at the original branching point persists even when the α/β fascicle is not bifurcated. When single cell clones are made in the ellipsoid body, mutant neurons fail to elaborate their axon projections within the ellipsoid body despite normal initial pathfinding.

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

    The dramatic overgrowth of presynaptic arbors found in hiwΔNterm mutant C4 da neurons is completely abolished in a Dscam118 MARCM clone background.

    The dramatic overgrowth of presynaptic arbors found in C4 da neurons expressing wndScer\UAS.cCa (under the control of Scer\GAL4ppk.PG) is completely abolished in a Dscam118 MARCM clone background.

    The mild overgrowth of presynaptic terminals in Fmr1Δ50M mutant C4 ddaC neuron clones is completely abolished by a Dscam118 mutant background.

    Xenogenetic Interactions
    Statement
    Reference

    Expression of Hsap\DSCAMDscam1.WT or Hsap\DSCAML1Dscam1.WT fails to rescue the axon segregation and additional sister branch defects of Dscam118/Dscam118 late pupal MB neuron clones.

    Complementation and Rescue Data
    Comments

    The dramatic reduction in presynaptic arbor growth in Dscam118 mutants is rescued by expression of Dscam1+t73.3.

    Expression of Dscam1C2.4.2-6.14-9.24-17.2, but not Dscam1C1.4.2-6.14-9.24-17.1, partially rescues the axon segregation and additional sister branch defects of Dscam118/Dscam118 late pupal MB neuron clones.

    Dscam4.3-6.36-9.25-17.1 fully rescues the projection neuron dendrite defects, but has no effect on the reduced number of calyx boutons seen in Dscam18 clones.

    Dscam4.3-6.36-9.25-17.2 partially rescues the reduced number of calyx boutons, but has no effect of the projection neuron dendrite defects seen in Dscam18 clones.

    The axon branching defects seen in single cell clones of mushroom body α/β neurons that are homozygous for Dscam18 are partially rescued by expression of Dscam4.3-6.36-9.25-17.2; only 9% of clones show lack of segregation of sister branches and only 21% show generation of additional branches at the bifurcation points (compared to 35% and 42% respectively in the absence of Dscam4.3-6.36-9.25-17.2).

    Dscam4.3-6.36-9.25-17.1 shows only minimal rescue of the axon branching defects seen in single cell clones of mushroom body α/β neurons that are homozygous for Dscam18; 28% of clones show lack of segregation of sister branches and 34% show generation of additional branches at the bifurcation points (compared to 35% and 42% respectively in the absence of Dscam4.3-6.36-9.25-17.1).

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    Synonyms and Secondary IDs (3)
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      References (5)