Pan-neuronal expression of the diffusible tutlGH15753.Scer\UAS isoform under the control of Scer\GAL4elav-C155 produces Fas2-positive tracks that crisscross the midline. The same phenotype is produced upon expression in the midline, driven by Scer\GAL4sim.PS.
Overexpression of tutlGH15753.Scer\UAS under the control of Scer\GAL4sca-109-68, Scer\GAL4how-24B or Scer\GAL4G14 produces excessive branching of the ISNd nerve, stalling of motor nerves, with some nerves, such as the transverse nerve, innervating muscles that are not their normal targets.
Overexpression of tutlGH15753.Scer\UAS in a wild-type background using the retina-specific Scer\GAL4GMR.PF produces neuronal defects in that many retinal axons stall before reaching their targets and some sprout extra axonal processes that can invade the cortex.
tutlGH15753.UAS/Scer\GAL4repo fails to rescue tutlex383
tutlGH15753.UAS/Scer\GAL4repo fails to rescue Df(2L)ed-dp/tutlex383
Post-mitotic neuronal expression of tutlGH15753.Scer\UAS under the control of either Scer\GAL4sim.PS or Scer\GAL4elav-C155 fully rescues the midline crossing defects found in tutlex383 and tutlex383/Df(2L)ed-dp mutants. Expression under the control of Scer\GAL4repo does not rescue the phenotype, indicating that expression near the midline is important for rescue.
Expression of tutlGH15753.Scer\UAS via Scer\GAL4elav-C155 can reduce the motor axon projection defects found in tutlex383 homozygotes.
Expression of either tutlGH15753.Scer\UAS driven by the pan-neuronal driver Scer\GAL4elav-C155 rescues most aspects of tutlk14703/tutlex383 mutant eye defects.
