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General Information
D. melanogaster
FlyBase ID
Feature type
Also Known As
IroDFM3, Df(3L)iroDFM3, Df(3)iroDFM3
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)
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
    NOT in combination with other aberrations

    Mutants show defects in the lateral larval muscle pattern. In more than 95% of cases muscles with lateral transverse (LT) morphology are absent. Instead, fibres with abnormal orientation appear in the lateral and ventral regions, but they never insert at LT attachment sites. Muscles DT1 and SBM develop with normal morphologies.

    Df(3L)iro-DFM3 mutant clones are easily recoverable in the ventral eye but do not have a visible phenotype. Small dorsal clones do not produce a strong morphological phenotype, large clones often lead to the formation of ectopic eye tissue near the dorsal head cuticle.

    Dorsal mutant R axons occasionally project to the ventral lamina in Df(3L)iro-DFM3 mutants.

    Homozygous clones in the eye result in enlargement of the dorsal eye. Eye discs homozygous for Df(3L)iro-DFM3 (generated using the "EGUF" method to remove all eye disc cells except the homozygous Df(3L)iro-DFM3 clone cells) show dorsal enlargement. Expression of PRAS40UAS.cCa under the control of Scer\GAL4ey.PH in eye discs homozygous for Df(3L)iro-DFM3 (generated using the "EGUF" method to remove all eye disc cells except the homozygous Df(3L)iro-DFM3 clone cells) results in a small eye phenotype due to a reduction of the eye on both dorsal and ventral eye margins in nearly 20% of flies. Expression of SerBd.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4ey.PH at 25oC in eye discs homozygous for Df(3L)iro-DFM3 (generated using the "EGUF" method to remove all eye disc cells except the homozygous Df(3L)iro-DFM3 clone cells) results in a complete loss of the eye in 99% of flies, compared to 50% of flies showing complete loss of the eye or a very small eye when SerBd.Scer\UAS.T:Hsap\MYC is expressed under the control of Scer\GAL4ey.PH at 25oC in a wild-type background.

    Df(3L)iro-DFM3 somatic clones generated in the dorsal rim of the eye still have specific dorsal rim ommatidia but also contain some non-dorsal rim ommatidia.

    Clones homozygous for Df(3L)iro-DFM3 induced during the first larval instar stage show conspicuous transformations of the dorsal head capsule. The most common transformation is a dorsal enlargement of the eye at the expense of the head capsule, or the appearance of ectopic eyes on the head capsule. Many of the clones that give rise to ectopic or enlarged eyes also show additional transformations of the dorsal cuticle to ventral structures, namely, ptilinum, suborbital bristles and prefrons and ectopic antenna and maxillary palpus structures (these structures also form a series, so that a clone displaying a given ventral structure in this series generally also shows those structures preceeding it in the series). The ectopic structures always appear as mirror images of the endogenous ones with a conserved dorsoventral arrangement. This causes the ventralmost ectopic structure, the maxillary palpus, to arise on the back of the head. The appearance of ectopic structures is accompanied by loss of dorsal capsule elements such as ocellar bristles and ocelli. Ectopic prefrons, antenna, rostral membrane and maxillary palpus structures formed in head capsules containing clones homozygous for Df(3L)iro-DFM3 consist exclusively of mutant tissue, while non-autonomous effects are seen in the wild-type head cuticle located between the endogenous and ectopic eye (the cuticle shows duplicate sets of supraorbital bristles in mirror-image arrangements), and in the ectopic eyes themselves. Transformations of head capsule are also seen in clones homozygous for Df(3L)iro-DFM3 that are are not associated with ectopic or enlarged eyes and are restricted to one or two types of ectopic ventral structure (ectopic ptilina and prefrons). These transformations are the most common in later-induced clones (induced 48-72 and 72-96 hours after egg laying). These late clones can also give rise to suborbital bristles or the most proximal part of the antenna. Clones homozygous for Df(3L)iro-DFM3 in the eye/antenna disc can be grouped into two categories. Firstly, clones where the general morphology of the disc is not affected and their size is roughly similar to that of their twin wild-type clone. Secondly, clones that show extra proliferation and form large outgrowths of mutant tissue. These clones arise from anterior/dorsal regions of the eye disc and always reach the disc margin. In the most extreme cases, these outgrowths can be recognised as complete or near complete duplications of the ventral parts of the eye disc and antenna disc.

    Homozygous Df(3L)iro-DFM3 (containing araDFM3, mirrDFM3 and removing caup) clone cause a series of phenotypes, adding progressively more 'ventral-type' tissue in the following order: dorsal eye overgrowth or ectopic dorsal eyes, overgrowth of ventral type of cuticle (ptilinum and rostral membrane) ectopic antennal pouches, antenna and maxillary palps. The extra head structures are produced autonomously, but the eyes can be composed of both mutant and wild-type ommatidia. The ectopic ventral structures, all grow from the orbital region of the head. The rest of the dorsal head is displaced by the over-grown tissue.

    Clones homozygous for Df(3L)iro-DFM3 (a deficiency for ara, caup and mirr) in the dorsal part of the eye which abut the eye disc margin are often associated with extensive outgrowths, which include both mutant and adjacent wild-type cells. A subset of these clones develop a clearly independent eye consisting of both mutant and wild-type cells. These mosaic eyes contain an ectopic equator, with wild-type ommatidia as far as 7 ommatidial rows away from the clonal border being repolarised towards it. Clones homozygous for Df(3L)iro-DFM3 in the dorsal head capsule cause autonomous transformations to ventral cuticle structures. Mutant cells in clones homozygous for Df(3L)iro-DFM3 in the dorsal part of the eye differentiate ommatidia normally, but they form compact patches with smooth borders, as if to minimise contact with surrounding cells. Clones in the ventral part of the eye disc have wiggly contours. Clones of dorsal origin are found in the ventral part of the eye disc. Such clones form straight boundaries with dorsal cells, but wiggly boundaries with ventral cells.

    Df(3L)iro-DFM1 and Df(3L)iro-DFM3 cell clones in the notum have indistinguishable phenotypes. Clones of cells homozygous for Df(3L)iro-DFM1 or Df(3L)iro-DFM3 in the notum induced during the first or second larval instar show malformations. Notum is transformed to wing hinge, with sclerites and tegula-like cuticle with characteristic sensory structures. Surrounding wild type cells are recruited into the ectopic structures. Ectopic axillary sclerites were always in mirror image disposition to the regular ones. Malformations in the more central region of the notum caused failure of fusion of the heminota. Clones in the third instar wing disc organize a fold around themselves, similar to the fold found between the notum and wing hinge parts of the regular wing disc.

    When homozygous, in wing clones, differentiation of L5 and the alula fail. Dorsal clones remove L5 dorsally, and ventral clones remove L5 ventrally. The dorsal component of L3, and part of L1, the L3-associated sensilla campaniformia, the sensillum of anterior crossvein and the TSM sensilla are removed. No other site in the wing showed a requirement for ara-:-caup. Notum cells lacking ara and caup are inviable.

    Stocks (1)
    Notes on Origin
    Balancer / Genotype Variants of the Aberration
    Separable Components
    Other Comments
    Synonyms and Secondary IDs (10)
    References (25)