Imprecise excision of vavKG02022 results in a 2293bp deletion of the vav locus. Neighbouring genes CG8010 and rictor are intact.
2293 bp deletion resulting from the imprecise excision of P{SUPor-P}VavKG02022. Upstream endpoint at insertion site inferred from map.
Somatic clones (induced specifically in the eye) of Vav3 homozygous cells in pupal retina display supernumerary cells in ommatidia (including cone cells and primary pigment cells).
The regular hexagonal lattice of pupal retina is disorganized in homozygous Vav3 mutants and contain extra cells of all types (inter-ommatidial cells, primary pigment cells as well as cone cells).
Vav3 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 Vav3 mutant eye discs compared to wild-type controls.
The presence of supernumerary accessory cells in Vav3 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.
Vav3 mutants display defect in ommatidial cluster rotation in third instar larval eye disc.
Cells in Vav3 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 vav3 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".
vav3 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 vav3 embryos. On average two longitudinal axons are misrouted across the midline in each embryo.
The midline glia is present in vav3 embryos.
Induction of clones in the photoreceptors of vav3 third instar larvae leads to axon mistargeting, whereas when clones are induced in the glial cells axon targeting occurs correctly.
Vav3 has increased cell number | pupal stage phenotype, enhanceable by shgk03401
Vav3 has increased cell number | pupal stage phenotype, suppressible by spi1
Vav3 has partially lethal - majority die phenotype, non-suppressible by trioUAS.cBa/Scer\GAL4arm.PS
Vav3 has partially lethal - majority die phenotype, non-suppressible by trioUAS.cBa/Scer\GAL4αTub84B.PL
Vav3 is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4GMR.PU, aosUAS.cUa
Vav3 has retina | pupal stage phenotype, enhanceable by shgk03401
Vav3 has primary pigment cell | pupal stage | increased number phenotype, enhanceable by shgk03401
Vav3 has cone cell | pupal stage | increased number phenotype, non-enhanceable by shgk03401
Vav3 has retina | pupal stage phenotype, suppressible by spi1
Vav3 has cone cell | increased number | pupal stage phenotype, suppressible by spi1
Vav3 has primary pigment cell | increased number | pupal stage phenotype, non-suppressible by spi1
Vav3/Vav[+] is an enhancer of retina | pupal stage phenotype of Scer\GAL4GMR.PU, cindrRNAi.PC.PD.UAS
Vav3/Vav[+] is an enhancer of primary pigment cell | pupal stage | increased number phenotype of Scer\GAL4GMR.PU, cindrRNAi.PC.PD.UAS
Vav3 is a suppressor | partially of eye phenotype of Scer\GAL4GMR.PU, aosUAS.cUa
The supernumerary cone cells in pupal retina characteristic for Vav3 allele 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 Vav3 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 Vav3 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 Vav3.
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 vav3 male homozygotes.
Vav3 is rescued by Scer\GAL4arm.PS/VavUAS.Tag:HA
Vav3 is rescued by VavUAS.Tag:HA/Scer\GAL4αTub84B.PL
Vav3 is partially rescued by Scer\GAL4arm.PS/VavUAS.Tag:HA
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 vav3 male homozygotes.
Expression of vavScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4arm.PS partially rescues the midline crossing phenotype seen in vav3 homozygotes.