UAS-transgene overexpression in lola-/- MARCM clones results in additive dendritic and axonal targeting defects. Representative images of (a) control and (b-e) experimental conditions as indicated for the vNB (1), DL1 single-cell dendrite (2) and axon (3) phenotypes of UAS-lola A (c), UAS-lola L (d) and UAS-lola T (e) expression in lola-/- MARCM clones. None of the transgenes are able to rescue the lola-/- phenotype. Expression of either UAS-lola A and UAS-lola T both result in a decrease in dendrite elaboration. (f) Quantification of vNB phenotypes. Data are presented as percentage of observed clones that innervate a particular target. UAS-lola transgenes fail to rescue the lola-/- phenotype. Often transgene expression has an additive effect and further disrupts normal targeting, for example, there are dramatic losses of VA1lm targeting with UAS-lola A and UAS-lola T. 'N' for rescue experiments are low due to extreme difficulty in generating MARCM UAS-expression clones in a lola-/- background. (g) Quantification of DL1 dendrite phenotypes as in Figure 5. UAS-lola L and UAS-lola T clones lack normal dendritic targeting. (h) Quantification of DL1 axonal phenotypes as in Figure 2. UAS-lola L and UAS-lola T show increases in axonal defects compared with lola-/- alone. anti-CD8::GFP in green, anti-nc82 neuropil in magenta. Scale bar, 20 μm.