Imprecise excision of vavKG02022 results in a 1532p deletion of the vav locus. Neighbouring genes CG8010 and rictor are intact.
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.
Vav2 has increased cell number | pupal stage phenotype, enhanceable by shgk03401
Vav2 has abnormal neuroanatomy | embryonic stage 17 phenotype, enhanceable by trio6A
Vav2 has abnormal neuroanatomy | embryonic stage 17 phenotype, enhanceable by Sose2H
Vav2 has increased cell number | pupal stage phenotype, suppressible by spi1
Vav2 has partially lethal - majority die | male limited | pupal stage phenotype, non-suppressible by trioUAS.cBa/Scer\GAL4arm.PS
Vav2 has partially lethal - majority die | male limited | pupal stage phenotype, non-suppressible by trioUAS.cBa/Scer\GAL4αTub84B.PL
Vav2 is an enhancer of abnormal neuroanatomy | embryonic stage 17 phenotype of trio6A
Vav2 is an enhancer of abnormal neuroanatomy | embryonic stage 17 phenotype of Sose2H
Vav2 is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4GMR.PU, aosUAS.cUa
Rap1rvB1, Vav2 has abnormal neurophysiology | larval stage phenotype
Adcy1rut-1, Vav2 has abnormal neurophysiology | larval stage phenotype
Vav2 has retina | pupal stage phenotype, enhanceable by shgk03401
Vav2 has primary pigment cell | pupal stage | increased number phenotype, enhanceable by shgk03401
Vav2 has larval longitudinal connective | embryonic stage 17 phenotype, enhanceable by trio6A
Vav2 has commissure | embryonic stage 17 phenotype, enhanceable by trio6A
Vav2 has larval longitudinal connective | embryonic stage 17 phenotype, enhanceable by Sose2H
Vav2 has commissure | embryonic stage 17 phenotype, enhanceable by Sose2H
Vav2 has NMJ bouton | larval stage | increased number phenotype, non-enhanceable by Scer\GAL4elav-C155/Rap1V12.UAS.Tag:MYC
Vav2 has cone cell | pupal stage | increased number phenotype, non-enhanceable by shgk03401
Vav2 has retina | pupal stage phenotype, suppressible by spi1
Vav2 has cone cell | increased number | pupal stage phenotype, suppressible by spi1
Vav2 has NMJ bouton | increased number | larval stage phenotype, non-suppressible by Scer\GAL4elav-C155/Rap1V12.UAS.Tag:MYC
Vav2 has primary pigment cell | increased number | pupal stage phenotype, non-suppressible by spi1
Vav2/Vav[+] is an enhancer of retina | pupal stage phenotype of Scer\GAL4GMR.PU, cindrRNAi.PC.PD.UAS
Vav2/Vav[+] is an enhancer of primary pigment cell | pupal stage | increased number phenotype of Scer\GAL4GMR.PU, cindrRNAi.PC.PD.UAS
Vav2 is an enhancer of larval longitudinal connective | embryonic stage 17 phenotype of Sose2H
Vav2 is an enhancer of commissure | embryonic stage 17 phenotype of Sose2H
Vav2 is an enhancer of larval longitudinal connective | embryonic stage 17 phenotype of trio6A
Vav2/Vav[+] is a suppressor of NMJ bouton | larval stage | decreased number phenotype of Rap1V12.UAS.Tag:MYC, Scer\GAL4elav-C155
Vav2 is a suppressor | partially of eye phenotype of Scer\GAL4GMR.PU, aosUAS.cUa
Abl4, Vav2 has embryonic/larval neuromuscular junction | larval stage phenotype
Abl4, Vav2 has NMJ bouton | increased number | larval stage phenotype
Abl4, Vav2 has macropinosome | larval stage phenotype
Rap1rvB1, Vav2 has embryonic/larval neuromuscular junction | larval stage phenotype
Rap1rvB1, Vav2 has NMJ bouton | increased number | larval stage phenotype
Rap1rvB1, Vav2 has macropinosome | larval stage phenotype
Adcy1rut-1, Vav2 has embryonic/larval neuromuscular junction | larval stage phenotype
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.
Vav2 is rescued by Scer\GAL4arm.PS/VavUAS.Tag:HA
Vav2 is rescued by VavUAS.Tag:HA/Scer\GAL4αTub84B.PL
Vav2 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 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.