FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\pod1Δ96
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General Information
Symbol
Dmel\pod1Δ96
Species
D. melanogaster
Name
FlyBase ID
FBal0154743
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Caused by aberration
    Cytology
    Description
    Mutations Mapped to the Genome
    Curation Data
    Type
    Location
    Additional Notes
    References
    Variant Molecular Consequences
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
    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

    A low but significant frequency of axon defects are found in embryonic motor neurons, consistent with a defect in axon targeting. Hemizygotes show guidance defects in 1.4%, 8.1% and 6.9% in ISN, SNa and ISNb neurons respectively. No defects are seen in neuroblast polarity, mitotic spindle orientation, cell fate determination, or epidermal integrity are seen. In maternal and zygotic nulls, embryos display a range of abnormalities in their VNC axons: thinning of longitudinals, abnormal midline crossing and wandering trajectories, axon tangles, axon breaks, collapse or thinning of the anterior and posterior commissures and defasciculation. 25.3%, 55.0% and 60.1% of ISN, SNa and ISNb neurons show guidance defects respectively. The ISN display defects such as stalling/splaying defasciculation, and failure to innervate targets. The SNa exhibit missing or truncated dorsal lateral branching, ar abnormal defasciculation. ISNb axons often dislay abnormalities such as failure to innervate the clefts between muscles 6/7 and 12/13, premature arrest, failure to defasciculate from the ISN and bypass of targets.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Phenotype Manifest In
    Additional Comments
    Genetic Interactions
    Statement
    Reference
    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Partially rescued by
    Comments
    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
    pod1Δ96
    Name Synonyms
    Secondary FlyBase IDs
      References (1)