Expression of fra::roboScer\UAS.RF.T:Hsap\MYC with Scer\GAL4Cha.7.4 leads to a severe depletion or absence of cholinergic axons in the commissures, efficiently displacing cholinergic axon terminals out of the dorsal motor neuropile. Under these conditions contact of motorneuron dendrites with cholinergic interneuron terminals is severely reduced and potentially absent at 18.5 hours after egg laying, unlike in the wild-type; yet the overall organisation of the neuropile, including the distribution of Fas2-positive tracts, is not affected. Dendritic intermediate (MN-LL1) and lateral (MN-DA3) territories also remain distinct, though they appear more variable compared to controls.
Expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav.PLu results in longitudinal tracts crossing the midline in embryos.
Expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav-C155 results in Fas2-positive axon bundles ectopically crossing the midline in the embryonic central nervous system. The embryos have an average of 0.86 crossovers/segment, with an average of 9.3 defects/embryo. The penetrance of this phenotype is 100%.
Expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav.PLu results in axon guidance defects in the central nervous system and reduced viability.
When driven in the neurons by Scer\GAL4elav.PLu, fra::roboScer\UAS.RF.T:Hsap\MYC causes a robo-like phenotype; too many axons cross the midline, resulting in thick fuzzy commissures and thin longitudinal tracts. This phenotype becomes stronger with more copies of fra::roboScer\UAS.RF.T:Hsap\MYC and Scer\GAL4elav.PLu. At higher levels a phenotype is seen that is much stronger than seen in robo mutants and is approaching that seen in sli mutants; the CNS axons appear to have partially collapsed onto the midline. When driven by the pan-mesodermal Scer\GAL4 line Scer\GAL4how-24B, a number of phenotypes are seen. Muscle precursors are observed extending towards and across the midline. These cells also have abnormal morphology, sending out many long thin filopodia and flattened lamellipodial extensions towards the sli expressing midline, suggesting that they are now attracted to sli. Muscles at a distance from the midline develop quite normally.
The longitudinal tract phenotype of double mutant NetAunspecified NetBunspecified embryos is not altered by expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav.PLu.
Gef64CEP3035 dramatically enhances the axon guidance defects caused by expression of fra::roboScer\UAS.RF.T:Hsap\MYC under the control of Scer\GAL4elav.PLu, leading to a significant increase in ectopic midline crossing.