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General Information
D. melanogaster
FlyBase ID
Feature type
Also Known As
Df(2)PC4, Df(PC4)
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

bk1 << E(var)55 << bk2 << l(2)08717

Genetic mapping information

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

Comments on Cytology

Ref: Lindsley and Zimm, 1992

Left limit of break 1 from polytene analysis (FBrf0080145) Right limit of break 1 from inclusion of grh (FBrf0041708) Left limit of break 2 from polytene analysis (FBrf0080145) Right limit of break 2 from non-inclusion of l(2)08717 (FBrf0067338)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Completely deleted / disrupted
Partially deleted / disrupted
Molecular Data
Completely deleted
Partially deleted
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

    Inferred to overlap with: Df(2R)BSC399.

    Enhancer of In(1)wm4h position-effect variegation.

    NOT in combination with other aberrations

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

    The Df(2R)PC4 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(2R)PC4 results in 4.8% X chromosome nondisjunction and 5.8% fourth chromosome nondisjunction in In(1)FM7/X ; svspa-pol females.

    Homozygous embryos have abnormal gut morphology.

    Does not cause unconditional lethality in hybrid females when heterozygous with D.simulans chromosome.

    Weak second site non-complementing phenotype with zipEbr (though not zipmhc-c6.1 : malformed phenotype penetrance 10-24%.

    Shows no maternal enhancement of dpphr4.

    Shows a dose-sensitive interaction with pbhs.PB.

    Uncovers Dsim\jba in D.melanogaster/D.simulans hybrids. Does not uncover Dsim\pm in D.melanogaster/D.simulans hybrids.

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

    Deficient embryos show a variably penetrant mutant midgut phenotype: variable constrictions absent.

    Homozygous embryos are very abnormal compared to wild-type and tracheae are not completely connected. Midgut constrictions do not form and Malpighian tubules are poorly differentiated.

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

    Semiviable over subDub. Transheterozygotes tend to die during the pupal phase or only eclose halfway. Escapers show rough eyes, etched tergites and blistered or nicked wings. Males and females are sterile.

    Fewer larger nuclei.

    Stocks (3)
    Notes on Origin
    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (8)
    References (104)