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General Information
Symbol
Dmel\sliunspecified
Species
D. melanogaster
Name
FlyBase ID
FBal0086336
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

    In sliunspecified mutant embryos, all axons collapse on the midline.

    The longitudinal tracts are collapsed at the midline in mutant embryos.

    The fascicles of the longitudinal connectives are fused at the midline in mutant embryos. Nearly all ganglionic branches are misrouted and branches do not migrate in the same dorsoventral plane. 17% of ganglionic branches stall outside or inside the central nervous system and 37% cross the midline. The migration of dorsal tracheal branches towards the heart is disrupted in stage 16 mutant embryos. 20% of the branches are either completely missing or stalled at various lengths. 28% of the fusion events that normally interconnect the tracheal network over the dorsal midline are disrupted. All primary visceral branches grow towards the gut in mutant embryos, but the migration of the secondary branches appears irregular in some embryos, with some projections extending more dorsally or ventrally along the midgut than normal.

    The heterozygote Df(1)NP5 phenotype is not enhanced in embryos also heterozygous for sliunspecified. In contrast, the frequency of midline guidance errors is increased in sliunspecified/+ embryos also heterozygous for Df(1)NP5. sliunspecified, in trans to a deficiency uncovering sli, such as Df(2R)Jp4 or Df(2R)Jp1 has complete midline fusion of all axon tracts. The semidominant interaction of sliunspecified and scbunspecified is also observed in sliunspecified/Df(2R)XTE-18 embryos.

    In contrast to wild-type, the nuclear division and cytokinesis of GMC-1 in sli mutant embryos is symmetric producing two nuclei of equal sizes.

    Embryos show collapse of axon fascicles at the central nervous system midline.

    sli null mutants show a characteristic collapse of all axons onto the central nervous system midline.

    No gross dentritic defects are seen in mutant embryos.

    Collapsed CNS axon phenotype with frequent breaks in the longitudinal connectives. Midline glial cells become displaced ventrally during stage 12 onward.

    sliunspecified mutant embryos show abnormal head involution. Abdominal transformations occur in combination with Pc like mutants.

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

    sliunspecified has phenotype, non-enhanceable by kuz[+]/kuzunspecified

    NOT suppressed by
    Statement
    Reference
    Enhancer of
    Other
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    The positioning of the longitudinal tracts in sliunspecified ; NetAunspecified NetBunspecified double mutant embryos is as seen in NetAunspecified NetBunspecified mutant embryos.

    Longitudinal tracts collapse at the midline in sliunspecified robounspecified double mutant embryos.

    The frequency of midline crossing is much higher in mewM6/Y;sliunspecified/+ and ifk27e/Y;sliunspecified mutants and also involves more lateral tracts. The semidominant interaction of sliunspecified and scbunspecified is also observed in sliunspecified/Df(2R)XTE-18 embryos. Tigx has a semidominant interaction with sliunspecified, Fas2 labelling of fascicles between segments is reduced and midline guidance defects are observed in one in three segments. LanA9-32 mutants, when double heterozygous with sliunspecified, exhibit midline crossover of Fas2-labelled axons in over 30% of segments. The degree of defasciculation and midline guidance errors in all axon tracts of the triple heterozygote of scbunspecified/sliunspecified;LanA9-32/+, appears to be additive of the individual phenotypes. In addition, a narrowing of the central nervous system and the medial displacement of all axon tracts is also seen in this mutant combination.

    Fas2-positive axons cross the central nervous system midline in about 12% of sliunspecified kuzunspecified double heterozygotes, in contrast to either single heterozygote. kuzunspecified homozygotes that are also heterozygous for sliunspecified have a central nervous system (CNS) phenotype similar to kuzunspecified single mutants, but the position of the longitudinal connectives is shifted towards the CNS midline. Removal of one copy of kuz+ in a sliunspecified homozygous background does not enhance the sli mutant phenotype.

    The addition of communspecified to sliunspecified mutants has no effect on the sliunspecified phenotype.

    Commissures are formed in communspecified sliunspecified double mutant embryos but in an irregular pattern.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Comments

    Expression of sliScer\UAS.cUa under the control of Scer\GAL4sli.PS rescues the midline crossing phenotype seen in sliunspecified, but does not restore proper lateral position of the FasII-positive fascicles.

    Expression of sliUncleave.Scer\UAS under the control of Scer\GAL4sli.PS rescues the midline crossing phenotype seen in sliunspecified, but does not restore proper lateral position of the FasII-positive fascicles.

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    Mutant
    Wild-type
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    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (1)
    Reported As
    Symbol Synonym
    sliunspecified
    Name Synonyms
    Secondary FlyBase IDs
      References (14)