FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Vav2
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General Information
Symbol
Dmel\Vav2
Species
D. melanogaster
Name
FlyBase ID
FBal0263789
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

Imprecise excision of vavKG02022 results in a 1532p deletion of the vav locus. Neighbouring genes CG8010 and rictor are intact.

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
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

The regular hexagonal lattice of pupal retina is disorganized in homozygous Vav2 mutants and contain extra cells of all types (inter-ommatidial cells, primary pigment cells as well as cone cells).

Vav2 homozygous mutants display extra photoreceptor cells in third instar larval eye disc (R7 and R8) as well as in the majority of ommatidia (supernumerary R7 photoreceptor cells) in a pupal retina. Precocious recruitment of R7 cells is observed in Vav2 mutant eye discs compared to wild-type controls.

The presence of supernumerary accessory cells in Vav2 homozygous pupal ommatidia does not correlate with the presence of extra R7 photoreceptor cells and the numbers of extra cone cells also do not correlate with the number of primary pigment cells.

Vav2 mutants display defect in ommatidial cluster rotation in third instar larval eye disc.

Cells in Vav2 homozygous somatic clones display defects in adherens junction dynamics and excessive cell movements (revealead by live imaging) which result in a patterning delay. The dynamics defects correlate with the recruitment of extra primary pigment cells.

The majority of vav2 homozygous mutants die at the pupal stages but male escapers exist. The escapers are wild type in appearance but exhibit locomotor defects and die shortly after eclosion. They have impaired spontaneous activity and a "shaking phenotype".

vav2 pupae that fail to eclose contain fully developed flies that exhibit severe locomotor defects.

Defects in axon projection are seen in approximately 14% of stage 17 vav2 embryos. On average two longitudinal axons are misrouted across the midline in each embryo. This phenotype is not enhanced when the maternal vav product is absent.

The midline glia is present in vav2 embryos.

63% of vav2 male homozygotes exhibit axon growth defects in the adult ellipsoid body, although the severity of the phenotype varies. In milder mutants only the external ring remains open whereas in more severe mutants both rings are open.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
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Reference
Suppressor of
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Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Suppressed by
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Reference
NOT suppressed by
Enhancer of
Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

The supernumerary cone cells in pupal retina characteristic for Vav2 mutants is almost completely suppressed by combination with spi1 in heterozygous state but the increased number of primary pigment cells remains unchanged.

The disorganised ommatidial lattice and supernumerary primary pigment cells phenotype characteristic for Vav2 homozygotes is strongly enhanced by combination with shgk03401 in heterozygous state but the proportion of ommatidia with extra cone cells is not further increased.

The patterning defects and mild supernumerary primary pigment cells phenotype observed in pupal retina of flies expressing cindrdsRNA.PC.PD.Scer\UAS under the control of Scer\GAL4GMR.PU can be significantly enhanced by combination with Vav2 in heterozygous state.

The small and rough adult eye phenotype seen in flies expressing aosScer\UAS.cUa under the control of Scer\GAL4GMR.PU can be partially restored by combination with Vav2.

Expression of trioScer\UAS.cBa under the control of either the Scer\GAL4arm.PS or the Scer\GAL4αTub84B.PL driver cannot suppress the semi-lethality seen in vav2 male homozygotes.

A large proportion of vav2 trio6A double mutant embryos exhibit gross patterning defects that make examination of axogenesis defects difficult. However in double mutant embryos that display less severe morphological defects the midline crossing phenotypes are enhanced compared to single mutants.

Homozygous Sose2H enhances the axon tract phenotypes seen in vav2 homozygous mutant embryos, with an increased number of midline crosses per embryo. No other CNS defects are observed.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of vavScer\UAS.T:Ivir\HA1 under the control of either the Scer\GAL4arm.PS or the Scer\GAL4αTub84B.PL driver rescues the semi-lethality seen in vav2 male homozygotes.

Expression of vavScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4arm.PS partially rescues the midline crossing phenotype seen in vav2 homozygotes.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (4)