R1-R6 growth cones scatter around the lamina termination region in third instar larvae where plexAdsRNA.Scer\UAS is expressed under the control of Scer\GAL4GMR.PF, leading to the appearance of a discontinuous termination layer in the lamina.
PlexARNAi.UAS, Scer\GAL4GMR.PF has eye photoreceptor cell | third instar larval stage phenotype, enhanceable by Df(2L)N22-5
PlexARNAi.UAS, Scer\GAL4GMR.PF has lamina | third instar larval stage phenotype, enhanceable by Df(2L)N22-5
PlexARNAi.UAS, Scer\GAL4GMR.PF is a suppressor of eye photoreceptor cell | third instar larval stage phenotype of Rho1N19.UAS, Scer\GAL4GMR.PF
PlexARNAi.UAS, Scer\GAL4GMR.PF is a suppressor of lamina | third instar larval stage phenotype of Rho1N19.UAS, Scer\GAL4GMR.PF
Reducing the dose of Sema-1a through the presence of Df(2L)N22-5 significantly enhances the plexAdsRNA.Scer\UAS knockdown phenotype (where expression is controlled by Scer\GAL4GMR.PF). The penetrance of the phenotype is increased from around 20% to approximately 60%, consistent with the idea that plexA and Sema-1a function in the same pathway.
The severity of the Rho1N19.Scer\UAS axonal-hyperfasciculation phenotype is significantly suppressed by knockdown of plexAdsRNA.Scer\UAS (with both transgenes under the control of Scer\GAL4GMR.PF).
PlexARNAi.UAS is rescued by PlexARNAi.UAS/Scer\GAL4GMR.PF
Expression of plexAΔcyt.Scer\UAS in R-cells where endogenous plexA is knocked-down by expression of plexAdsRNA.Scer\UAS (both transgenes under the control of Scer\GAL4GMR.PF) largely restores the R1-R6 termination pattern in the lamina.