Figure 1.

A screen to uncover new players of ddaC pruning. Live imaging of ddaC neurons labeled by ppk-GAL4 expressing UAS-CD8-GFP. A–C, A timeline of ddaC pruning. Z-projections of dorsal abdominal body wall at 0 (A), 10 (B), and 18 h APF (C), respectively. At 10 h APF, almost all the branches are severed close to the soma. By 18 h APF, the severed dendrites are cleared, only the soma and axon remain. D, Scheme showing the genes known to be involved in ddaC pruning; arrows represent direct interactions. E, The expression of EcR-RNAi^CA104 in ddaC robustly blocks the early stages of ddaC pruning. Dendritic branches are not severed at 18 h APF. F, Interaction screen: flies carrying ppk-GAL4, UAS-CD8-GFP, and a null mutation for EcR are crossed with balanced deficiencies. Pupal dominant markers on balancer chromosomes allow the selection of the appropriate genotypes. The F₁ pupae trans-heterozygous for EcR and a deficiency are imaged at 18 h APF and assessed for defects in pruning. G–I, ddaC neurons from pupae trans-heterozygous for EcR and three different deficiencies at 18 h APF. G, In category i of F₁ pupae, pruning is normal, meaning that there is no genetic interaction. H and I show F₁ pupae in which genetic interactions are evident. H, In category ii, clearance defects occur and pieces of dendrite are still in the field at 18 h APF; severing does not appear to be affected. I, In category iii, severing and clearance defects are evident with some dendrites still attached to the soma. J–L, Identification of the gene responsible for pruning defects within the deficiency Df(3R)ED6332. J, Trans-heterozygous neuron for Df(3R)ED6332 and EcR at 18 h APF. K, RNAi-15532R2, which targets headcase (hdc), one of the genes removed by Df(3R)ED6332, at 18 h APF. L, Genetic interaction between EcR and hdc⁴³, a null allele of hdc, at 18 h APF.