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General Information
D. melanogaster
Deficiency (3R) Delta
FlyBase ID
Feature type
Also Known As
DlFX3, Df(3R)DlFX3, Df(3R)FX3, Df(3R)DlFX3
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 << l(3)91Fa << Dl << bk2

Genetic mapping information
Comments on Cytology

All limits from polytene analysis (FBrf0046377)

Sequence Crossreferences
DNA sequence
Protein sequence
Gene Deletion and Duplication Data
Genes Deleted / Disrupted
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

    Mutant embryos show an overproduction of muscle founder cells.

    Before delamination of the SI neuroblasts, medial, intermediate and lateral regions of the neuroectoderm can be detected in homozygous embryos. Only slight differences in cell size can be detected in the ventral neuroectoderm (VNE) compared to wild-type. However, morphological changes are visible in the basal regions of the VNE; in contrast to wild type, where only single basally enlarged cells can be detected, whole groups of cells become larger basally in homozygous embryos. The enlarged cells also do not shrink during stage 9 as occurs in wild-type embryos, rather more and more cells become enlarged until almost all cells of the VNE have increased in size and eventually become neuroblasts.

    Single cells from wild-type embryos transplanted into the ventral neurogenic region of Df(3R)Dl-FX3 host embryos give rise to neural cells.

    Heterozygotes show a 'delta' phenotype and confluence of wing veins 2 and 5.

    Embryos exhibit few, if any, fused muscles. The unfused, birefringent fibres, have a random pattern of fine fibres apparently radiating out from small fragments of dorsal cuticle. The birefringent is clearly correlated with the expansion of the CNS and PNS, and the loss of epidermis and the degree to which myoblast fusion occurs. Where myoblast fusion fails conspicuous clusters of mesodermal cells are formed and if epidermal territories are expanded cells in these clusters may be recruited to fusion.

    Homozygotes die as embryos. Surface of the CNS at 20 hours almost completely lacks investing cells. Islands of neural lamella and associated sheath cells are observed but no continuous barrier cell layer. There are few glial profiles among the abundant neuron cell bodies within the ganglion and among neurons in the neuropile.

    Post-transcriptional control of AS-C expression is suppressed, all cells expressing RNA accumulate protein.

    The expression of the Df(3R)Dl-FX3 phenotype is modified by the presence of ASC loss-of-function mutations.

    Fusion of tarsal segments: 2-4 tarsal segments fuse together forming a single segment without boundaries visible.

    Homozygotes die as embryos with an extreme embryonic neurogenic phenotype.

    Stocks (0)
    Notes on Origin
    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (9)
    References (35)