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General Information
D. melanogaster
FlyBase ID
Feature type
Also Known As
Df(2L)32FP5, Df(2L)5, Df(5), salDf(2L)32FP5
Computed Breakpoints include
Sequence coordinates
2L:11,450,129..11,454,221 [-] (Df(2L)32FP-5:bk2)
Member of large scale dataset(s)
Nature of Aberration
Cytological Order
Class of aberration (relative to wild type)
Class of aberration (relative to progenitor)


Carries alleles
Transposon Insertions
Formalized genetic data
Genetic mapping information
Comments on Cytology
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

    In combination with T(2;3;4)FCK-25, the anterior notopleural macrochaetae are not formed.

    NOT in combination with other aberrations

    The lateral muscle pattern is normal in mutant larvae.

    Homozygous clones in the adult retina have ommatidia with extra photoreceptors and ommatidia with altered chirality.

    Heterozygotes have a small delta in the distal part of wing vein L4 and show a modest reduction in wing size compared to wild type.

    Homozygous clones induced early in the wing disc do not grow if they are located where normally notum tissue would develop, resulting in roundish wing discs in these cases. Large homozygous clones are recovered in the wing primordium, and survive within the notum if induced later in development.

    Df(2L)32FP-5 clones generated along the A/P boundary of the wing imaginal disc, using the FLP/FRT technique, show no defects in segregation behaviour. As with wild-type clones, these mutant clones stay in the compartment in which they have been generated.

    Mosaic ommatidia in animals containing homozygous clones have defects in planar cell polarity with chirality inversions and misrotations. In mosaic ommatidia which adopt the correct chiral form, the R3 cell is always salm+ and salr+. In mosaic ommatidia which adopt the wrong chiral form, the R4 cell is always salm- and salr-. In mosaic ommatidia in which only the R3 precursor is salm- and salr- incorrect and correct chirality are seen at about the same frequency. Mosaic ommatidia containing symmetric R4/R4 or R3/R3 configurations are also seen and in each case, at least one cell of the R4/R3 pair is salm- and salr-. In homozygous clones in the eye, most ommatidia have eight large and no small rhabdomeres.

    Homozygous embryos show autocellular adherens junctions throughout the tracheal system and a lack of the multicellular dorsal branch.

    Homozygous embryos have a normal number of glial cells, although they have a less regular distribution and are more rounded than normal.

    Homozygous mutant clones in the antenna exhibit cuticular defects. In homozygous clones the circular outline of the joint between antennal segments 2 and 3 is defective.

    No large phenotypic changes are detected in the photoreceptor cells (PRCs) in mutant imaginal discs and the projections to the optic lones appear to be normal. However the mutant ommatidia in the adult eye are greatly altered: The small central rhabdomeres of inner R7 and R8 PRCs are absent, and extra PRCs with large rhabdomeres are observed. R7 and R8 cells exhibit features of outer R1-R6 PRCs in a cell autonomous manner. In addition, a small proportion of ommatidia are seen with as many as nine or ten outer photoreceptor rhabdomeres, which appear to arise both from rhabdomere duplication and from recruitment of additional PRCs.

    No dorsal trunk forms in the tracheal system in homozygous embryos.

    Large mitotic clones of cells homozygous for Df(2L)32FP-5 (which uncovers both salm and salr) result in reorganisations of the venation pattern that are manifest both within and outside the salm/salr domain of expression. Small clones localized between the veins L2 and L3, and between L4 and L5 cause autonomous formation of ectopic vein tissue, irrespective of the wing surface where the clones appear. The differentiation of L3 and L4 is not affected in these clones, rather these veins are displaced. Clones in the anterior compartment can also differentiate ectopic sensilla characteristic of L3. All clones that span wing vein L2 result in the elimination of this vein.

    Homozygotes die as embryos.

    Homozygous clones in the thorax are viable and of normal size. The anterior and the posterior notopleural bristles are absent, and the posterior scutellar and the posterior dorsocentral bristles are displaced to the anterior. The seven remaining macrochaetae are unaffected. The differentiation of microchaetae is normal.

    Mitotic clones in the wing exhibit disappearance, displacement, fusion and ectopic formation of specific veins as well as reductions in wing size.

    Stocks (1)
    Notes on Origin

    Selected as: ry- revertant.

    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (14)
    References (37)