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General Information
D. melanogaster
Deficiency (3L) Adelaide Carpenter
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)
Causes alleles
Carries alleles
Transposon Insertions
Formalized genetic data

Rdl << bk1 << eIF-4E << l(3)67BDa << bk2 << can

Genetic mapping information

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

Comments on Cytology

Limits of break 1 from polytene analysis (FBrf0076124) Left limit of break 2 from polytene analysis (FBrf0099762) Right limit of break 2 from polytene analysis (FBrf0076124)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Partially deleted / disrupted
Molecular Data
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(3L)BSC282.

    Inferred to overlap with: Df(3L)BSC283.

    Df(3L)AC1 suppresses the position effect variegation of the mutant Sb phenotype which is seen in the T(2;3)SbV chromosome.

    Does not show a dose-sensitive interaction with Df(3R)Ubx109.

    NOT in combination with other aberrations

    The salivary gland distal tip does not initiate turning and migration in embryos homozygous for Df(3L)AC1 by stage 14.

    Flies heterozygous for the deletion show a Minute bristle phenotype.

    In Df(3L)AC1 homozygous embryos, the macrophages migrate throughout the embryo, cluster in the vicinity of apoptotic cells and perform endocytosis of diI-AcLDLs as in controls.

    Df(3L)AC1 embryos show defects in tracheal cell migration.

    Heterozygotes have a suppressed eye phenotype compared to wild-type flies that have been exposed to UV irradiation.

    Heterozygosity for this deletion has no effects on achiasmate chromosome segregation.

    Dominantly suppresses the KrIf-1/+ eye phenotype.

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

    Weak second site non-complementing phenotype with zipEbr and zipmhc-c6.1 : malformed phenotype penetrance 10-24%.

    Shows no maternal enhancement of dpphr4.

    Shows a dose-sensitive interaction with pbhs.PB.

    Acts as a dosage sensitive maternal modifier of run : causes tergite defects in greater than 50% of run3 heterozygotes.

    Deficient embryos show a mutant midgut phenotype: central constriction absent.

    Homozygous embryos show abnormal head involution and tracheal formation. Formation and differentiation of the gut is variable.

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

    Fertile when heterozygous with haync2.

    Stocks (2)
    Notes on Origin



    Uncovered among progeny of males

    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments

    The Df(3L)AC1 chromosome may 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), but the eye colour phenotype in the presence of Df(3L)AC1 overlaps the eye colour phenotype in a wild-type background so it cannot be unequivocally demonstrated that the deficiency chromosome uncovers a suppressor of telomeric silencing.

    Synonyms and Secondary IDs (8)
    References (109)