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General Information
D. melanogaster
Deficiency (3R) ebony
FlyBase ID
Feature type
Also Known As
Df(3R)eF1, Df(3R)eF1
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

l(3)93Ca << bk1 << l(3)AFA7 << l(3)93Dk << bk2 << lbe

Genetic mapping information

Breakpoint(s) molecularly mapped

Comments on Cytology

Left limit of break 1 from non-inclusion of l(3)93Ca (FBrf0040940) Right limit of break 1 from inclusion of l(3)93Cb (FBrf0040940) Left limit of break 2 from inclusion of bap (FBrf0091087) Right limit of break 2 from non-inclusion of lbe (FBrf0091087)

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

    Df(3R)lb/Df(3R)e-F1 are uncovered for lbl, lbe and bap. In these embryos no dramatic change is seen in the ventral nerve cord morphology. However, there seem to be slightly more lateral projections compared to wild-type. The glial cell population is also affected in its positioning and number. An increased number of medially located glial cells is seen, as is a partial loss or abnormal positioning of lateral exit and subperineural glial cells. An additional ~2.3 glial cells are seen per hemineuromere. Defects are also seen i the segmental nerves. The distance between the ISN and SN bundles is much more variable and larger than seen in wild-type.

    bap null embryos (Df(3R)e-F1/Df(3R)e-D7 embryos carrying tin+t10.7, referred to as "bapDf") show visceral mesoderm defects; the presumptive visceral mesoderm cells do internalise, but they show incomplete coalescence of the clusters during stage 11. At later stages, very few of the visceral mesoderm cells are attached to the endoderm. Cells which originate from trunk visceral mesoderm primordia fuse into syncytia of somatic muscles.

    Df(3R)e-D7/Df(3R)e-F1 embryos carrying a tin rescue transgene have an increased number of somatic gonadal precursor cells.

    NOT in combination with other aberrations

    tin+t10.7 Df(3R)e-D7/Df(3R)e-F1 embryos lack muscle fibres at the position of the segmental border muscle (SBM) and have unfused myoblasts in or around the SBM position in 57% of hemisegments. In the remaining 43% of hemisegments, the muscle fibres lying within or close to the segmental borders have abnormal shapes and have insertion sites clearly distinct from those of the SBM. The lateral adult muscle precursors are absent or reduced in number, and the ventral adult muscle precursors are duplicated.

    Homozygous embryos do not develop the anal plate and display defects in the dorsal cuticle. Anal plate is restored by heat induced expression of P{hs-lbl}.

    Stocks (2)
    Notes on Origin
    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments

    Primer targetted to lbe shows it is located outside the deleted region but lack of lbe activity in homozygous embryos suggests the chromosome carries an additional mutation in lbe or deletes some regulatory sequences located downstream of the gene.

    Synonyms and Secondary IDs (4)
    References (32)