Expression of robo1ΔC.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PLu in embryos results in ectopic crossing of the midline by Fas2-positive axons in approximately one-third of segments.
Overexpression of roboΔC.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PLu leads to defects in longitudinal axon guidance. About 2.2. defects are seen per animal and about 20% of segments exhibit defects.
Single copies of robo1ΔC.Scer\UAS.T:Hsap\MYC driven by either Scer\GAL4elav.PLu or Scer\GAL4ftz.ng produce no detectable phenotype. When two copies are driven by Scer\GAL4elav.PLu, axons of the medial-most Fas2 expressing longitudinal pathway can be seen inappropriately crossing the midline. A similar but weaker phenotype is seen when robo1ΔC.Scer\UAS.T:Hsap\MYC is driven by Scer\GAL4ftz.ng.