FB2025_01 , released February 20, 2025
Aberration: Dmel\Df(3R)swp2MICAL
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General Information
Symbol
Df(3R)swp2MICAL
Species
D. melanogaster
Name
FlyBase ID
FBab0029816
Feature type
Also Known As
MicalDf(3R)swp2
Computed Breakpoints include
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Class of aberration (relative to progenitor)
Breakpoints
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data
Genetic mapping information
Comments
Comments on Cytology
Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Partially deleted / disrupted
Molecular Data
Completely deleted
Partially deleted
Genes NOT Deleted / Disrupted
Complementation Data
 
Molecular Data
 
Genes Duplicated
Complementation Data
Completely duplicated
Partially duplicated
Molecular Data
Completely duplicated
Partially duplicated
Genes NOT Duplicated
Complementation Data
 
Molecular Data
 
Affected Genes Inferred by Location (0)
    If no genes are listed here, it may be because the affected region is very large. The JBrowse insert above may show an error for the same reason, and other FlyBase tools such as CytoSearch may also fail for large regions. You can contact FlyBase for more help.
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    Phenotypic Data
    In combination with other aberrations

    Fails to complement: Df(3R)by62.

    Fails to complement: Df(3R)mr73.

    Fails to complement: Df(3R)mrO1.

    41.9% of hemisegments in Df(4)C3/+ ; Df(3R)swp2MICAL/+ double heterozygotes show defects in muscle 6/7 innervation and 33.0% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 44.6% of hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24.

    NOT in combination with other aberrations

    Homozygous embryos show guidance and innervation defects in the SNa pathway (46.2% of hemisegments show defects compared to 11.2% in wild-type embryos).

    Homozygotes survive to larval stages and have no obvious morphological abnormalities. There are no obvious somatic muscle defects and the overall architecture of the PNS and CNS is normal.

    Homozygotes survive to larval stages and have no obvious morphological abnormalities.

    68.9% of homozygous hemisegments show defects in muscle 6/7 innervation and 57.3% show defects in muscle 12/13 innervation (these defects in ISNb axons include axons stalling, bypassing targets and absent or decreased muscle innervation). 81.2% of homozygous hemisegments show SNa pathway defects, failing to make the two characteristic turns between muscles 22 and 23 and muscles 23 and 24. Prominent guidance defects are also seen in axons that give rise to the ISNd, SNc, TN and the third most lateral Fas2-positive longitudinal connective in the CNS.

    Stocks (0)
    Notes on Origin
    Discoverer
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (6)
    Reported As
    Name Synonyms
    Secondary FlyBase IDs
      References (15)