Imprecise excision of vavKG02022 results in a 1460bp deletion of the vav locus. Neighbouring genes CG8010 and rictor are intact.
The majority of vav1 homozygous mutants die at the pupal stages but male escapers exist. The escapers appear wild type but exhibit locomotor defects and die shortly after eclosion. They have impaired spontaneous activity and a "shaking phenotype".
vav1 pupae that fail to eclose contain fully developed flies that exhibit severe locomotor defects.
Defects in axon projection are see in approximately 14% of stage 17 vav1 embryos. On average two longitudinal axons are misrouted across the midline in each embryo.
The midline glia is present in vav1 embryos.
All vav1 third instar larvae show some disruption to photoreceptor targeting. Some regions of the lamina neuropil are hyperinnervated by R1-R6 photoreceptors whilst others lack innervation. Axonal defects are also seen in the medulla, ranging from a total lack of medullar innervation to an increase in the number of neurons entering the medulla region compared to wild type.
The number and distribution of laminal glial cells in the optic lobe of vav1 third instar larvae is comparable to wild type.
The R2-R5 subset of axons, which stalls in the lamina neuropil in wild type third instar larvae, migrates towards the medulla in vav1 mutants.
Vav1 is not rescued by VavUAS.Tag:HA/Scer\GAL4GMR.PU
Expression of vavScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4GMR.PU fails to rescue the photoreceptor targeting phenotype seen in vav1 homozygotes.
