Expression of Sema1aScer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PLu in embryos does not induce significant increase in axon pathfinding defects relative to controls.
Scer\GAL4elav.PLu/Sema1aUAS.Tag:MYC is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of Scer\GAL4elav.PLu, pblUAS.N.Tag:HA
Scer\GAL4elav.PLu/Sema1aUAS.Tag:MYC is a non-enhancer of larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype of Scer\GAL4elav.PLu, pblUAS.N.Tag:HA
Scer\GAL4elav.PLu/Sema1aUAS.Tag:MYC is a non-enhancer of axon | embryonic stage phenotype of Scer\GAL4elav.PLu, pblUAS.N.Tag:HA
The moderate axon pathfinding defects (defasciculation defects in intersegmental nerve b motor axons very infrequent lateral axon tract disruptions in the central nervous system) characteristic for embryos expressing pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu are not exacerbated by co-expression of Sema1aScer\UAS.T:Hsap\MYC.
Scer\GAL4sca-537.4/Sema1aUAS.Tag:MYC partially rescues Sema1ak13702
Expression of Sema1aScer\UAS.T:Hsap\MYC under the control of Scer\GAL4sca-537.4 strongly rescues the axon guidance defects characteristic for Sema1ak13702 homozygous embryos - the defects in the central nervous system are strongly suppressed but the frequency of defasciculation irregularities in the intersegmental nerve b is only mildly decreased.