The eye morphology defects (rough appearance with fused ommatidia) characteristic for flies expressing cazVDRC.cUa under the control of Scer\GAL4GMR.PS can be rescued by co-expression of HsrωdsRNA.Sym.Scer\UAS and further worsened by co-expression of HsrωEP93D (which on its own also causes eye defects).
Third instar larvae simultaneously expressing both HsrωdsRNA.Sym.Scer\UAS and cazVDRC.cUa under the control of Scer\GAL4elav.PLu display crawling ability deficiency as well as morphological defects in the neuromuscular junctions (reduced total synaptic branch length and number of boutons) but the severity of each of these defects is not significantly different from either of the single knockdowns.
The decrease in the number of synaptic boutons in Scer\GAL4elav.PLu>cazVDRC.cUa-expressing larvae is significantly enhanced by TER94k15502/+. However, there is significant differences in the size of synaptic boutons among these genotypes.
Total branch length phenotype caused by Scer\GAL4elav.PLu>cazVDRC.cUa in motor neurons is significantly suppressed by the co-expression of TER94Scer\UAS.cHa. The number of synaptic boutons is also significantly increased in Scer\GAL4elav.PLu>cazVDRC.cUa larvae co-expressing TER94Scer\UAS.cHa compared with larvae expressing Scer\GAL4elav.PLu>cazVDRC.cUa alone.