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General Information
Symbol
Dmel\enE
Species
D. melanogaster
Name
FlyBase ID
FBal0049458
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
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

The deletion extends from 9.6kb upstream of the en transcription start site to 31.7kb downstream, deleting about half of the inv transcription unit.

Df(2R)enE breaks at approximate coordinate 0 and -50 in the inv-en region, removing most of the en and inv transcription units, including all of the insertion from enXho25.

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
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Large homozygous clones induced in late third larval instar gonads are often associated with a disorganised terminal filament. Large terminal filament clones in the pupal ovaries are also associated with a failure to properly organise the terminal filament stack. Smaller posterior terminal filament cell clones have no detectable effect on terminal filament stack organisation.

Stage 15 enE embryos have only ~13 genital disc precursor cells, instead of the wild-type number of 22.

Stigmatophores do not form in enE mutants.

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.

Fails to complement the adult phenotype of en1. Causes extreme embryonic segmentation defects: its denticle belts fused into an almost continuous lawn.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Suppressor of
Statement
Reference

enE is a non-suppressor of decreased cell number | embryonic stage phenotype of ptc9

Other
Statement
Reference
Phenotype Manifest In
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Approximately 60% of fra1/enE double mutants exhibit defects in axonal pathfinding. Stage 15 embryos display dramatic defects in ventral nerve cord architecture, with the posterior commissures missing or fused with the anterior commissures, and longitudinal tracts thinner. Nearly all the segments are affected in these embryos.

Stage 15 enE ptc9 embryos have increased levels of genital disc precursor cells, similar to levels seen in ptc9 single mutants.

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 wgl-17 double mutant embryos have segmentally repeated denticle whorls.

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
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

Partially complements: obk1. Fails to complement the wing venation defects of obk1 but complements the antennal duplication and eye bristle phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (29)