Open Close
General Information
D. melanogaster
Deficiency (3R) blistery
FlyBase ID
Feature type
Also Known As
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)


Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data
Genetic mapping information
Comments on Cytology

There is no evidence of a 2:3 translocation. The rearrangment at 85D-F looks like a typical, conventional deficiency.

The description of Df(3R)by62 as a deficient translocation in FBrf0051508 was an error propagated from a typographical error in FBrf0069831. The original cytological description has been retrieved from the laboratory notebook of Ken Kemphues where the deficiency is clearly described as a transposition segregant.

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

    In Fmr1Δ83M/Df(3R)by62 pharate adults, the α and β lobes appear very immature, resembling those seen in wild-type brains at earlier stages of metamorphosis. In many cases, the lobes appear younger than those of pupae whose β lobe fibers are just approaching the midline. The mushroom body α/β immaturity phenotype is characterised by abnormally thin α and β lobes that are very irregular along their lengths, whereas the γ lobes appear normal. Approximately 80-90% of Fmr1Δ83M/Df(3R)by62 brains show α/β immaturity. Over 90% of the mushroom bodies of Df(3R)by62 heterozygotes are immature, confirming the dominant effect of the deficiency. The severity of the Df(3R)by62 α and β lobe immaturity phenotype is ehanced by Fmr1Δ83M.

    Fails to complement: Df(3R)swp2MICAL. Fails to complement: Df(3R)swp4. Fails to complement: Df(3R)swp7. Fails to complement: Df(3R)swp11. Fails to complement: Df(3R)swp38.

    NOT in combination with other aberrations

    The Df(3R)by62 chromosome acts as a dominant moderate 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

    Shows dominant enhancement of dominant haltere phenotype caused by Ubx195 and Ubx9.22.

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

    No second site non-complementing phenotype with zipEbr and zipmhc-c6.1.

    Shows no maternal enhancement of dpphr4.

    Does not show a dose-sensitive interaction with pbhs.PB.

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

    Suppressor of the dosage dependent (two or more copies of P{sev-svp1} or P{sev-svp2}) transformation of cone cells into R7 photoreceptors and at a lower frequency R7 cells into outer photoreceptors.

    Deficient embryos show an uninterpretable mutant midgut phenotype.

    Homozygous embryos show defects in cell divisions.

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

    Embryonic lethal.

    Stocks (1)
    Notes on Origin
    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (6)
    References (73)