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General Information
D. melanogaster
FlyBase ID
Feature type
Also Known As
Df(1)scB57, scB57, Df(1)scB57
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

bk1 << Exp6 << bk2

Genetic mapping information

Shown to have left breakpoint between y and ac and right breakpoint just to the right of that of Df(1)260-1.

Comments on Cytology

Interstitial deletion.

All limits from inclusion of l(1)1Bb (citation unavailable)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
Complementation Data
Partially deleted / disrupted
Molecular Data
Completely deleted
Partially deleted
Genes NOT Deleted / Disrupted
Complementation Data
Molecular Data
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
    NOT in combination with other aberrations

    Homozygous embryos have a significantly reduced number of pericardial cells and lymph gland blood progenitors compared to wild type, as well as a small decrease in the number of cardioblasts.

    Mutant stage 14 embryos have the same number of posterior midline glia per segment as wild-type controls.

    Homozygous intestinal stem cell clones grow similarly to wild-type clones and do not show defects in intestinal stem cell maintenance.

    Df(1)sc-B57 mutants are homozygous lethal. Df(1)sc-B57/+ mutants show loss of the posterior supra-alar, posterior notopleural, anterior notopleural and anterior postalar bristles to varying degrees.

    Combining Df(2L)GR4 (which removes the ASC: Achaete-scute Complex) and ato1 causes the loss of most cells in the embryonic peripheral nervous system (PNS) - only the two dorsal located md neurons remain.

    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. Bristle loss is greater at 25oC than at 18oC. In female D.simulans/D.melanogaster hybrids heterozygous for pnrVX6 and Df(1)sc-B57, the posterior and anterior scutellar bristles and the posterior and anterior dorsocentral bristles are lost at a high frequency compared to female D.simulans/D.melanogaster hybrid with pnrVX6 or Df(1)sc-B57 alone.

    Malpighian tubule tip cells are absent in homozygous embryos.

    Embryos lack most brain neuroblasts.

    SNSPs are reduced or absent. Typically a single, large SNS pouch, which may be branched, invaginates from the stomodeal epithelium.

    Loss of neuron mutant.

    In embryos lacking the AS-C, large basophilic midgut cells are absent and the number of adult midgut precursors is strongly reduced. No cell death accompanies the losses suggesting that the cells that would have developed as large basophilic midgut cells and adult midgut precursors develop as principal midgut epithelial cells instead. The resulting midgut epithelium is structurally normal. Double mutants with Dl9P have normal midgut epithelium, but the large basophilic midgut cells are missing and the number of adult midgut precursor cells are reduced.

    Df(1)sc-B57 mutants express normal levels of dpn in their reduced number of neuroblasts. Females doubly heterozygous for Df(1)sc-B57 and a heat shock dpn contruct, and heat shocked during pupation, have many missing bristles.

    Homozygous embryos have a smaller, more disorganised ventral nerve cord than normal, with noticeable thinning in areas along the nerve cord.

    20--25% of neuroblasts are absent in homozygous Df(1)sc-B57 embryos due to commitment of fewer cells. Neuroblasts in the medial and lateral rows are preferentially affected. Neuroblasts that succeed in segregating are smaller than wild type. The median neuroblast and midline precursor cell MP2 are missing. The death of cells that have segregated from the neuroectoderm and their progeny contribute to the neural hypoplasia.

    Stocks (4)
    Notes on Origin
    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (5)
    References (48)