UAS regulatory sequences drive expression of ptc coding sequences.

ptc^UAS.cMa/Scer\GAL4^hs.PB rescues ptc^unspecified

Scer\GAL4^arm.PS/ptc^UAS.cMa partially rescues ptc^unspecified

Maternally-derived expression of ptc^Scer\UAS.cMa under the control of Scer\GAL4^arm.PS in a ptc^unspecified mutant background rescues the formation of NB4-2 and specification defects in as many as 60% of hemisegments. With Fas2 staining, guidance defects were rescued in 80% of hemisegments. Staining with BP102 revealed 60% rescue of guidance defects per segment, indicating that not all of the neuroblasts that contribute to commissural tracts were rescued. When Scer\GAL4^arm.PS is paternally-derived, neither the NB4-2 defects nor the medial tract guidance defects in ptc^unspecified mutants are rescued.

Expression of ptc^Scer\UAS.cMa under the control of Scer\GAL4^hs.PB for 30 minutes at 37^oC results in a near complete rescue of the longitudinal tracts in ptc^unspecified embryos. Medial tracts are normal in 93% of hemisegments. Even when there is mis-routing of the medal tracts, only a few growth cones appear to be crossing the midline. These rescues are only observed when the ptc^Scer\UAS.cMa transgene is induced between 2 and 3 hours of development. No rescue is observed with the induction of ptc^Scer\UAS.cMa during other developmental time points. A 10 minute induction of the ptc^Scer\UAS.cMa transgene partially rescues the defects, whereas a 20 minute induction results in a very strong rescue. These results indicate that the presence of ptc protein in a narrow time window during the specification of neuroblast identity is sufficient to rescue the medial axon tract defects in ptc^unspecified mutant embryos.