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General Information
Symbol
Dmel\Ablunspecified
Species
D. melanogaster
Name
FlyBase ID
FBal0089849
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
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 ( 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

    Mutant embryos have axons ectopically crossing the midline in the central nervous system.

    Embryos which are derived from homozygous female germline clones but are paternally rescued have relatively normal central nervous system development, with occasional collapsed longitudinal axons and gaps in axon bundles. Embryos lacking both maternal and zygotic Abl function have severe disruptions in central nervous system development. Most show loss of commissural axons and some have defects in both longitudinal and commissural axons. Embryos lacking both maternal and zygotic Abl function show striking defects in the cellular events of dorsal closure. Leading edge cells do not elongate uniformly and some cells have overly broad or narrowed leading edges. Cells lateral to the leading edge elongate (as occurs in wild type), but do so nonuniformly. Some cells completely fail to change shape. The epithelial sheets often fail to align properly at the midline once dorsal closure is complete. Some mutants initiate dorsal closure even though they have not completed germband retraction. Some cells in the embryos become multinucleate due to defects in cellularisation. Actin enrichment is not uniform at the leading edge during dorsal closure. Dorsal closure is substantially slowed in embryos lacking both maternal and zygotic Abl function, taking two to three times longer than normal. The dorsal/ventral extent of the amnioserosa is larger in the mutant embryos compared to wild type. As closure proceeds, the leading edge of the lateral epidermis folds under the more lateral cells that follow it, suggesting that the leading edge cells do not migrate towards one another at an appropriate rate. Filopodial extensions from epidermal and amnioserosa cells are present in the mutant embryos.

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

    Central nervous system axons are seen to cross the midline in Ablunspecified capt06955 double heterozygous embryos.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Images (0)
    Mutant
    Wild-type
    Stocks (0)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (1)
    Reported As
    Symbol Synonym
    Ablunspecified
    Name Synonyms
    Secondary FlyBase IDs
      References (7)