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General Information
D. melanogaster
Deficiency (3L) Wrinkled
FlyBase ID
Feature type
Also Known As
Df(3L)WR4, Df(3L)Wr4, Df(3L)w+R4
Computed Breakpoints include
Sequence coordinates
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

Eip75B << bk1 << W << ads << bk2 << l(3)j13B3

Genetic mapping information

This deletion removes a single ribosomal protein-coding gene (though other genes are also removed).

Breakpoint(s) molecularly mapped

Comments on Cytology

Limits of break 1 from polytene analysis (FBrf0074960) Left limit of break 2 from polytene analysis (FBrf0051843) Right limit of break 2 from non-inclusion of l(3)j13B3 (FBrf0067338)

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

    Loss of heterozygosity is elevated compared to wild-type in Df(3L)x37/Df(3L)W4 animals. Df(3L)x37/Df(3L)W4 animals have macrochaetae defects (probably due genomic instability resulting in the loss of genetic material at haploinsufficient Minute loci).

    NOT in combination with other aberrations

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

    The Df(3L)W4 chromosome does not act as a dominant suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{wvar}KR3-2", a stable "brown-red" variant of the P{3'WP-2,wvar}2Lt insertion).

    Heterozygosity for Df(3L)W4 results in 0.7% X chromosome nondisjunction and 0.3% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.

    Dominantly enhances the KrIf-1/+ eye phenotype.

    Shows no maternal enhancement of dpphr4.

    Midgut development of mutant embryos is wild type.

    Homozygous embryos are very abnormal compared to wild-type.

    Heterozygosity for this deletion suppresses the mutant ovarian phenotype of ovoD2.

    Number of cells expressing midline glial cell markers in the embryonic CNS is increased by 60%.

    Homozygotes show the full cell death defective phenotype.

    75B puff is unchanged.

    Stocks (2)
    Notes on Origin


    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (13)
    References (43)