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General Information
Symbol
Dmel\invE
Species
D. melanogaster
Name
FlyBase ID
FBal0045909
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
    Nature of the Allele
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    Df(2R)enE breaks at approximate coordinate 0 and -50 in the inv-en region.

    Deletion removing the C-terminal three exons of inv.

    Caused by aberration
    Expression Data
    Reporter Expression
    Additional Information
    Statement
    Reference
     
    Marker for
    Reflects expression of
    Reporter construct used in assay
    Human Disease Associations
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Disease
    Evidence
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    Modifiers Based on Experimental Evidence ( 0 )
    Disease
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    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Disease-implicated variant(s)
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In
    Detailed Description
    Statement
    Reference

    Con-positive longitudinal fascicles and commissures are grossly disturbed in Df(2R)enE embryos (carrying both enE and invE). The muscles are grossly abnormal.

    enE invE double mutant clones of posterior origin show a variety of phenotypes in the wing. Clones distant from the A/P compartment boundary induce outgrowths and duplications both in and adjacent to the clones. Posterior clones at the A/P boundary sometimes cross into or displace the A/P boundary, while others straddle the normal site of the A/P restriction. Outgrowths and ectopic or disrupted venation are sometimes seen at the site of the normal A/P boundary. In a few rare cases, clones appear to obey the A/P lineage restriction from the posterior side. Posterior clone cells that have crossed or displaced the A/P boundary do not associate normally with anterior cells.

    Embryos fail to complete embryogenesis: defects are more extreme than for simple en mutant, en8 or simple inv allele, inv30.

    External Data
    Interactions
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    Phenotypic Class
    Phenotype Manifest In
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    Df(2R)enE mutant embryos (carrying both invE and enE) completely lack hindgut boundary cell rows and rings.

    Neuroblast NB 7-3 is missing in 100% of Df(2R)enE hemisegments (in which embryos are mutant for both en and inv).

    Df(2R)enE embryos (which are mutant for both en and inv) show slight overgrowth of the hindgut, although its overall morphology is almost normal. The border cells of the hindgut (which normally form an anterior and posterior ring at the ends of the hindgut and bilateral strands that connect the two rings) do not differentiate in these embryos.

    Df(2R)enE clones (mutant for both en and inv) of posterior origin in the wing disc sort, when in contact with anterior cells, into anterior territory. Df(2R)enE; ci94 double mutant clones of anterior origin in the wing disc straddle the anterior/posterior (A/P) boundary, similar to ci94 single mutant clones. Unlike Df(2R)enE single mutant posterior clones, however, Df(2R)enE; ci94 double mutant clones of posterior origin only partially sort into anterior territory and straddle the A/P boundary (similar to ci94 or Df(2R)enE; ci94 clones originating in the anterior compartment). Df(2R)enE; ci94 double mutant clones of both anterior and posterior origin define straight borders with neighbouring wild-type anterior and posterior cells. Df(2R)enE; ci94 double mutant clones show smooth borders with adjacent wild-type cells when situated entirely within the posterior compartment. Unlike Df(2R)enE single mutant clones, Df(2R)enE smo3 double mutant clones of posterior origin in the wing disc invariably occupy only posterior territory and define straight borders to anterior cells at the normal position of the anterior/posterior (A/P) boundary. Df(2R)enE smo3 double mutant clones of anterior origin also occupy posterior territory and define straight borders to anterior cells at the normal position of the A/P boundary.

    The specification of the majority of tendon cells is eliminated in Df(2R)enE embryos. Some muscles in these embryos have abnormal free ends.

    enE invE embryos have duplicated RP2 neurons in several hemisegments. This is due to the transformation of the NB5-3 neuroblast to a NB4-2 fate. enE invE embryos expressing wghs.PN, or enE invE Df(2R)gsb triple mutants have triplicated RP2 neurons. The triplication in enE invE Df(2R)gsb embryos is due to transformation of the NB5-3 and NB5-6 neuroblasts to a NB4-2 fate. gsbhs.PBH prevents the duplication of RP2 neurons seen in enE invE embryos when expressed during stage 8. ptc9 enE invE triple mutants lack RP2 neurons.

    Xenogenetic Interactions
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    Complementation and Rescue Data
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    Mutant
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    Stocks (1)
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    Synonyms and Secondary IDs (1)
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      References (15)