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General Information
Symbol
Dmel\LarE55
Species
D. melanogaster
Name
FlyBase ID
FBal0048850
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

    Deficiency breakpoint maps between exons 3 and 4 and deletes the 5' portion of the Lar gene.

    Caused by aberration
    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

    ISNb axons often show a "bypass" phenotype (failing to enter the normal muscle target domain just outside the ventral nerve cord and instead following the intersegmental nerve towards dorsal targets) in Larbypass/LarE55 embryos.

    Truncation phenotypes of the ISN. Most ISNs reach PT1 (persistent twi cell 1) but have small terminal arbors. Combining Ptp69D or Ptp99A mutants increases the penetrance and severity of the ISN defects, the ISN pathway is truncated at specific branchpoint positions. Triple mutants lacking Lar, Ptp69D or Ptp99A exhibit much stronger ISN phenotypes than any single or double mutant. Mutation affects SNb guidance and synaptogenesis within the VLM (ventrolateral muscle) field, a parallel bypass phenotype is observed (SNb axons grow alongside the ISN). SNbs fail to form the normal pattern of synaptic branches and exhibit navigation errors at the muscle field entry point. Growth alongside the ISN is likely to be due to inappropriately active Ptp99A rather than a failure of Lar-mediated VLM recognition. Penetrance of the parallel bypass phenotype of the mutation is beyond the levels observed in null mutants, penetrance is still reduced by Ptp99A mutants. Lar, Ptp69D or Ptp99A triple mutants also exhibit fusion bypass phenotype of the SNb axons. Fusion bypass is seldom observed in any genotype in which Ptp69D is wild type. Removal of Ptp99A or Lar produces a 10- to 20- fold increase in the frequency of fusion bypass and an increase in complete stall phenotypes.

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

    The Larbypass/LarE55 ISNb "bypass" phenotype is suppressed by Abl1, Abl2 or Abl4. The ISNd bypass phenotype of Larbypass/LarE55 embryos is also suppressed by Abl1.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Comments
    Images (0)
    Mutant
    Wild-type
    Stocks (2)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (1)
    Reported As
    Symbol Synonym
    LarE55
    Name Synonyms
    Secondary FlyBase IDs
      References (3)