FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\vvldfr-E82
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General Information
Symbol
Dmel\vvldfr-E82
Species
D. melanogaster
Name
FlyBase ID
FBal0035926
Feature type
allele
Associated gene
Dmel\vvl
Associated Insertion(s)
Carried in Construct
Also Known As
dfrE82
Key Links
Allele class

loss of function allele

Mutagen
Nature of the Allele
Allele class

loss of function allele

(Anderson et al., 1996, Anderson et al., 1995, de Celis et al., 1995)
Mutagen
ethyl methanesulfonate
(Anderson et al., 1996, Certel et al., 1996, Anderson and Johnson, 1995, Anderson et al., 1995)
Progenitor genotype
Cytology
Description

553bp deletion in the 5' untranslated region.

(Anderson et al., 1996)

5' untranslated sequences from +20 to +572bp are deleted.

(Certel et al., 1996)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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

      embryonic/larval ganglionic tracheal branch | embryonic stage 15

      (Sonnenfeld et al., 2010)

      embryonic/larval tracheal dorsal trunk | embryonic stage

      (de Celis et al., 1995)

      embryonic/larval tracheal section | embryonic stage

      (Sonnenfeld et al., 2010)

      embryonic/larval tritocerebral commissure | embryonic stage 14

      (Meier et al., 2006)

      filzkorper

      (de Celis et al., 1995)

      glial cell

      (Anderson and Johnson, 1995)

      glial cell & embryonic brain | embryonic stage 14

      (Meier et al., 2006)

      larval deutocerebrum | embryonic stage 14

      (Meier et al., 2006)

      larval longitudinal connective

      (de Celis et al., 1995)

      larval longitudinal connective | embryonic stage 14

      (Meier et al., 2006)

      larval protocerebrum | embryonic stage 14

      (Meier et al., 2006)

      larval tracheal system

      (Anderson et al., 1996, Anderson et al., 1995)

      larval tritocerebrum | embryonic stage 14

      (Meier et al., 2006)

      larval ventral nerve cord | embryonic stage 14

      (Meier et al., 2006)

      lobula | somatic clone

      (Hasegawa et al., 2011)

      macrochaeta | ectopic

      (de Celis et al., 1995)

      medulla layer M2 | somatic clone

      (Hasegawa et al., 2011)

      medulla layer M3 | somatic clone

      (Hasegawa et al., 2011)

      medulla layer M8 | somatic clone

      (Hasegawa et al., 2011)

      medulla layer M9 | somatic clone

      (Hasegawa et al., 2011)

      medulla layer M10 | somatic clone

      (Hasegawa et al., 2011)

      mesectoderm

      (Anderson et al., 1996)

      midline glial cell

      (Ma et al., 2000)

      presumptive embryonic/larval central nervous system

      (de Celis et al., 1995)

      presumptive embryonic/larval nervous system

      (Anderson et al., 1996)

      symmetrical commissure

      (Anderson and Johnson, 1995, Anderson et al., 1995, de Celis et al., 1995)

      tracheal lateral trunk anterior branch primordium | embryonic stage 15

      (Sonnenfeld et al., 2010)

      tracheal lateral trunk posterior branch primordium | embryonic stage 15

      (Sonnenfeld et al., 2010)

      tracheal metamere | embryonic stage

      (Sonnenfeld et al., 2010)

      tracheal section

      (de Celis et al., 1995)

      transmedullary neuron Tm27 | somatic clone

      (Hasegawa et al., 2011)

      ventral denticle belt

      (de Celis et al., 1995)

      wing

      (de Celis et al., 1995)

      wing & macrochaeta

      (de Celis et al., 1995)

      wing blade posterior compartment

      (de Celis et al., 1995)

      wing vein

      (de Celis et al., 1995)
      Detailed Description
      Statement
      Reference

      Compared with wild-type or heterozygous neurons, homozygous vvldfr-E82 mutant Tm27 neurons display reduced arborization at M8-10, ectopic arborization at M2-3, and axonal targeting defects in the lobula.

      (Hasegawa et al., 2011)

      In control stage 15 embryos, the anterior and posterior lateral trunks (Lta and Ltp, respectively) from adjacent segments are joined. In contrast, gaps occur between the Lta and Ltp in stage 15 homozygous vvldfr-E82 embryos.

      By stage 15, in control embryos, tracheal ganglionic cells and branches enter the ventral nerve cord (VNC) toward the central nervous system (CNS) midline. In contrast, in homozygous vvldfr-E82 embryos, tracheal ganglionic branches and cells rarely enter the VNC when present and are truncated, but in most cases are absent.

      Homozygous vvldfr-E82 embryos show significant losses in the continuity of tracheal tubules (gaps and breaks) and constrictions in the dorsal trunk. Dorsal branch formation does not occur in some metameres in homozygous vvldfr-E82 mutants.

      (Sonnenfeld et al., 2010)

      In stage 14 vvldfr-E82 homozygous embryos there is a gap separating the deutocerebral brain region from the neuromeres of the more posterior subesophageal ganglion. This phenotype is associated with severe axonal patterning defects in the embryonic central nervous system: the longitudinal connectives that normally run from the deutocerebral and tritocerebral neuromeres to the subesophageal ganglion are severely reduced or missing; the tritocerebral commissure, which interconnects the brain hemispheres at the level of the tritocerebrum, is completely absent; descending and ascending axons which normally project through the tritocerebrum in well formed fascicles, fail to do so; marker analysis suggests that there are general defects in the neural differentiation in the embryonic tritocerebrum; there are marked axonal patterning defects in the protocerebrum; organization of the subeosophageal ganglion and ventral nerve cord is disrupted. In addition, the pattern of glial cell localization is abnormal in brain regions with axonal patterning defects.

      (Meier et al., 2006)

      Some midline glia are misplaced from their normal positions in mutant embryos.

      (Ma et al., 2000)

      Homozygous embryos exhibit a severely disrupted tracheal phenotype with limited tracheal cell migration and absence of primary branch formation. P{hs-btl.M} induced expression (45 minute heat shock at 4 hours of development) restores the normal tracheal phenotype; extensive cell migration and several well-defined branches, formation of dorsal trunk and restoration of lateral branches. Ventral nerve cord defects associated with mismigration of mesectodermal progeny are not rescued.

      (Anderson et al., 1996)

      Embryos exhibit commissural defects and aberrantly localised midline glia in the ventral nerve cord. Also defects in tracheal cell migration leading to the absence of major tracheal branches.

      (Anderson and Johnson, 1995)

      Disruption of the developing tracheal tree and commissural defects in the developing CNS.

      (Anderson et al., 1995)

      Mutant embryos show reduced width of denticle belts (reminiscent of mutations in the spitz group of genes). Denticle belts are disturbed particularly in the third thoracic segment and the regular spacing of the commissures and connectives of the CNS is perturbed. Filzkorpers have abnormal shape suggesting that their connection to the tracheal trunk has failed. Dorsal trunk and branches of the tracheal system are lacking. Instead the tracheal pits form abnormal cavities that remain disconnected. Clones in the wing are smaller than controls and affect the differentiation of wing structures. In proximal regions they cause fusion of vein trunks and both dorsal and ventral clones autonomously fail to differentiate veins. The effect is restricted to the surface in which the clone lies. Dorsal clones in veins LIII and LIV cause both loss of and thickened vein, often resulting in folding of the wing. Ventral clones in the posterior compartment close to vein LIV can cause vein loss. Veins in the anterior wing margin are not affected. Dorsal and ventral clones between veins LIII and LV produce ectopic bristles, with features of wing margin bristles.

      (de Celis et al., 1995)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      In contrast to single heterozygous vvldfr-E82 or jing1 mutants, double heterozygous embryos show tracheal ganglionic branch defects.

      In contrast to single heterozygous vvldfr-E82 or jing3 mutants, double heterozygous embryos show tracheal ganglionic branch defects.

      jing3/vvldfr-E82 double heterozygotes show significant losses in the continuity of tracheal tubules (gaps and breaks) and constrictions in the dorsal trunk (Dt), similar to the homozygous phenotypes of jing3 and less severe than that of homozygous vvldfr-E82.

      Dorsal branches (Db-s) are absent, truncated or broken in jing3/pntΔ88 double heterozygotes.

      In contrast to each single heterozygote, abnormal Db boundary crossovers are observed in about 12% of metameres in jing1/vvldfr-E82 double heterozygotes.

      (Sonnenfeld et al., 2010)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      vvldfr-E82 is rescued by vvl+mAa

      (Anderson et al., 1995)
      Partially rescued by

      vvldfr-E82 is partially rescued by vvlUAS.cCa/Scer\GAL4NP2646

      (Hasegawa et al., 2011)
      Comments

      Expression of vvlScer\UAS.cCa under the control of Scer\GAL4CG11873-NP2646 partially rescues the Tm27 neuron phenotype of homozygous vvldfr-E82 clones.

      (Hasegawa et al., 2011)

      Mutant phenotype can be rescued by one copy of P{RX-dfr-minigene}.

      (Anderson et al., 1995)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (5)
      References (15)