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General Information
D. melanogaster
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

bk1 << pch << Exp6 << bk2 << svr

Genetic mapping information

Breakpoint(s) molecularly mapped

Comments on Cytology

Limits of break 1 from polytene analysis (FBrf0005951) Left limit of break 2 from inclusion of Cyp4g1 (FBrf0054051) Right limit of break 2 from polytene analysis (FBrf0005951)

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

    Fewer cells enlarge in the embryonic ventral neuroectoderm before delamination of the SI neuroblasts compared to wild-type embryos; 33% in the medial, 4% in the intermediate and 11% in the lateral region (wild-type numbers are 63%, 20% and 64% respectively). Prior to the delamination of the SII neuroblasts, when in the wild-type neurectoderm the cells of the intermediate regions enlarge, there is almost no increase in cell size in corresponding regions in Df(1)260-1 embryos.

    NOT in combination with other aberrations

    Df(1)260-1 clones in the wing margin produce bristles with an abnormal morphology.

    Thoracic Df(1)260-1 clones are devoid of bristles. Coexpression of sensUAS.cNa and daUAS.cGa, under the control of Scer\GAL4Eq, results in the formation of bristles in these clones.

    The bristle phenotype seen female D.simulans/D.melanogaster hybrids is significantly exacerbated by the Df(1)260-1 deletion, which removes the achaete-scute complex.

    The ventral cord of hemizygous embryos is strongly fragmented and all external sensory organs of the trunk are missing. Neural hypoplasia of the CNS and PNS are strongly reduced by Scer\GAL4da.G32-mediated expression of l(1)scUAS.cHa.

    Df(1)260-1 clones produce normal numbers of olfactory sensilla on the surface of the third antennal segment, although some of these sensilla are smaller than normal and are morphologically abnormal.

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

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

    Embryos lack all es organs but ch organs develop normally (FBrf0046281). P{hsp(sE)-poxn} expression can lead to the formation of external structures typical of es organs.

    Hemizygous clones in the labellum lack all taste bristles; the taste pegs as well as the pseudotracheal structures are absent.

    In heterozygous females the deletion acts as a dominant suppressor of h and emc. All es and most of the nd neurons are removed, ch neurons are not affected.

    Lethal in homozygous and hemizygous condition.

    male lethal somatic cell viable Germ-line clones lethal (Garcia-Bellido and Robbins, 1983, Genetics 103: 235-47). Eliminates all external sense organs in embryo (Dambly-Chaudiere and Ghysen, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 222-28).

    Stocks (2)
    Notes on Origin

    Demerec and Hoover, 1936.

    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (6)
    References (53)