FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\vvlGA3
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General Information
Symbol
Dmel\vvlGA3
Species
D. melanogaster
Name
FlyBase ID
FBal0044443
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
vvl6A3
Key Links
Mutagen
Nature of the Allele
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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
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Modifiers Based on Experimental Evidence ( 0 )
Disease
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Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Traheal migration is affected in vvlGA3 mutants. The cells form and then degenerate.

The lch5 neurons are situated in a more dorsal position than normal in 60-70% of abdominal segments in mutant embryos. If the lch5 neurons are situated just above the dorsal bipolar dendrite neuron, their dendrites point ventroposteriorly. The v'ch1 neuron is in its normal position. Mutant embryos show a loss of mild loss of es neurons. Many more apoptotic nuclei than normal are seen in the lateral clusters of the peripheral nervous system of mutant embryos. A small fraction of vvlM638/vvlGA3 animals develop to pharate adults which have bristle defects on the head thorax and abdomen.

Defects in tracheal invagination are seen in stage 12 embryos.

Loss of vein mutation. Suppression of rhohs.PSt ectopic vein phenotype and enhancement of the rhove-1 loss of vein phenotype.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

vvlGA3 mutants in a Df(3L)H99 background display defects in tracheal development. The primordia undergo epithelial-mesenchymal transition and migrate up to the primordia coalescence; however, the later dorsal migration does not progress.

Xenogenetic Interactions
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Complementation and Rescue Data
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Mutant
Wild-type
Stocks (0)
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (14)