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General Information
Symbol
Df(1)KA9
Species
D. melanogaster
Name
FlyBase ID
FBab0000486
Feature type
Also Known As
KA9
Computed Breakpoints include
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Progenitor
Mutagen
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

ben << bk1 << sesF << bk2 << eag

Genetic mapping information
Comments

This deletion removes multiple ribosomal protein-coding genes (in addition to other genes).

Comments on Cytology

Left limit of break 1 from polytene analysis (FBrf0080375) Right limit of break 1 from polytene analysis (FBrf0048204) Left limit of break 2 from polytene analysis (FBrf0086390) Right limit of break 2 from polytene analysis (FBrf0048204)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Genes NOT Deleted / Disrupted
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
    Phenotypic Data
    In combination with other aberrations
    NOT in combination with other aberrations

    Embryos hemizygous for Df(1)KA9 exhibit severe defects in the ventral nerve cord, with a near complete loss of midline crossing in some axon commissures; midline crossing of EW, EG and SP1 neurons is severely disrupted.

    Flies heterozygous for the deletion do not show a Minute bristle phenotype.

    The morphology of the proventriculus is normal in hemizygotes.

    Shows no maternal enhancement of dpphr4.

    Dominantly causes tergite defects in less than 50% of run3 heterozygotes.

    Embryos exhibit variable defects in the formation of commissural pathways. Scer\GAL4rho.PL induced expression of P{UAS-NETA} or P{UAS-NETB} significantly rescued the CNS phenotype.

    CNS defect in embryos: axon commissures are drastically thinner or missing amd the longitudinal tracts are highly disorganised and discontinuous. Commissural phenotype is only weakly rescued by expression of P{slit-NetA} or P{slit-NetB}.

    Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.

    Hemizygous embryos were examined with polarised light microscopy and antibody staining and found to have wild type muscle pattern and contraction.

    incomplete condensation and splitting of ventral nerve cord in hemizygous embryos

    Stocks (2)
    Notes on Origin
    Discoverer
     
    Balancer / Genotype Variants of the Aberration
     
    Separable Components
     
    Other Comments
     
    Synonyms and Secondary IDs (3)
    Reported As
    Name Synonyms
    Secondary FlyBase IDs
      References (39)