FB2024_03 , released June 25, 2024
Allele: Dmel\mmyslm
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General Information
Symbol
Dmel\mmyslm
Species
D. melanogaster
Name
FlyBase ID
FBal0335679
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Mutagen
    Nature of the Allele
    Mutagen
    Progenitor genotype
    Cytology
    Description

    Amino acid replacement: ?75term.

    Mutations Mapped to the Genome
    Curation Data
    Type
    Location
    Additional Notes
    References
    Nucleotide change:

    A6471442T

    Amino acid change:

    K75term | mmy-PD; K75term | mmy-PB; K112term | mmy-PA

    Reported amino acid change:

    ?75term

    Comment:

    Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

    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

    mmyslm homozygous embryos exhibit fully penetrant defects in the longitudinal connective only after 13/14h post-fertilization, when they show narrower axon bundles of longitudinal connectives, thicker commissures, which are also closer to one another, severe axon guidance defects of posterior corner cell neurons' longitudinal tracks, namely the M track inappropriately crossing the midline, the I and L tracks collapsing onto one another,and significant decreases in the thickness of these tracks and in their distance to the midline, as compared to controls.

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

    The defects in axon medial tracts observed in late mmyslm homozygous embryos are not suppressed by the expression of robo1Scer\UAS.cKa under the control of Scer\GAL4elav.PU.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Partially rescued by
    Comments

    The severe axon guidance defects at the longitudinal connective of late mmyslm homozygous embryos are partially and fully rescued by the expression of mmyScer\UAS.cMa under the control of Scer\GAL4sim.PU alone and in combination with Scer\GAL4elav.PU, respectively.

    Images (0)
    Mutant
    Wild-type
    Stocks (0)
    Notes on Origin
    Discoverer

    Identified as a background mutation associated with the Df(2L)fn7 chromosome in BDSC stock number 6067. The mmyslm mutation can be recombined away from the Deficiency.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (1)
    Reported As
    Symbol Synonym
    Name Synonyms
    Secondary FlyBase IDs
      References (1)