FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\sounspecified
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General Information
Symbol
Dmel\sounspecified
Species
D. melanogaster
Name
FlyBase ID
FBal0039961
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
unspecified
Key Links
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Progenitor genotype
    Cytology
    Description

    FlyBase curator comment: this entry is used to capture phenotypic information when the particular allele (or allele combination) used by the author could not be determined but the context of the experiment suggests that the phenotype being described is some kind of loss of function.

    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

    Loss of so function results in the absence of eye field derived neuroblast lineages including P5m.

    Axonal projections of the ato-expressing dorsal cluster lobular pattern appears essentially wild type in mutant brains.

    In mutant larvae the R7/R8 axons project to positions in the optic anlage consistent with their dorsoventral positions in the eye disc and independent of Bolwig's nerve.

    sounspecified has no effect on the period of CkIIβAnd flies.

    The number of photoreceptor cells is variably reduced in the nervous system of third instar larvae. In third instar larvae completely lacking photoreceptors, mitotically active lamina precursor cells are absent.

    Eyes are reduced to small groups of facets. Diacylglycerol kinase activity is very low compared to wild-type.

    Cell degeneration is seen in the optic lobes, the medulla cortex and the cortex of the lobula complex in the pupa.

    The number of axons in the anterior optic tract (AOT) is reduced by 35% compared to wild-type. sol1 sounspecified double mutants have a loss of up to 83% of axons in the AOT compared to wild-type.

    Most flies are completely eyeless, but some individuals have a variable number of facets on one or both sides. There is extensive cell degeneration in the medulla cortex and the cortex of the lobular complex in the pupa, and axon degeneration in the inner optic chiasma. The reduction in the medulla of the optic lobe in the adult is most severe in the distal region. There is no lamina. Many neuronal cell types found in the wild-type medulla and lobular complex are also found in so mutant flies.

    External Data
    Interactions
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    Phenotypic Class
    Phenotype Manifest In
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    Transheterozygotes with eya4 are normal.

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

    Ultrastructural analysis indicates that the sol1 and sounspecified mutations act independently on nearly exclusive subsets of axons in the AOT.

    The types of neural cell present in so mutant optic lobe rudiments has been investigated.

    Studies of gynandromorph flies show that the so mutation acts primarily on the eye anlagen. Cell degeneration occurs in the medulla after the axons have participated in the formation of the second optic chiasma.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (3)
    References (21)