Expression of robo110xScer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4elav.PLu in embryos results in strong inhibition of midline crossing in the ventral nerve cord, producing thin or absent commissures in nearly 100% of segments, and also results in disorganization of longitudinal axon pathways.
Expression of robo110xScer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4eg-Mz360 in embryos results in failure of EW neurons to cross the midline of the ventral nerve cord.
Commissure formation is strongly impaired in embryos expressing robo110xScer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4elav.PLu. No ectopic crossing of the midline by Fas2-positive axons is seen.
Expression of robo110xScer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4eg-Mz360 in embryos results in 97.1% of EW neurons failing to cross the midline.
Expression of robo110xScer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4sli.PS in embryos results in a mild ectopic midline crossing phenotype in the Fas2-positive axons.
Expression of robo110xScer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4eg-Mz360 in embryos results in the EW axons failing to cross the midline in almost all segments.
robo110xUAS.Tag:HA,Tag:SS(wg)/Scer\GAL4elav.PLu partially rescues robo11
Expression of robo110xScer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4elav.PLu rescues the FasII-positive axon guidance defects of robo11/robo11 mutants, but also causes additional axon guidance defects, including disruption of normal commissure formation and disorganization of longitudinal axon pathways.
Expression of robo110xScer\UAS.T:Ivir\HA1,T:SS-wg under the control of Scer\GAL4elav.PLu rescues the ectopic midline crossing phenotype seen in the medial Fas2-positive axons in robo11 embryos.