Genes controlling muscle size and survival play important roles in muscle wasting diseases. InDrosophila melanogastermetamorphosis, larval abdominal muscles undergo two developmental fates. While a doomed population is eliminated by cell death, another persistent group is remodelled and survives into adulthood. To identify and characterize genes involved in the development of remodelled muscles, we devised a workflow consisting ofin vivoimaging, targeted gene perturbation and quantitative image analysis. We show that inhibition ofTORsignalling and activation of autophagy promote developmental muscle atrophy in early, whileTORandyorkieactivation are required for muscle growth in late pupation. We discovered changes in the localization of myonuclei during remodelling that involve anti-polar migration leading to central clustering followed by polar migration resulting in localization along the midline. We demonstrate that the Cathepsin L orthologueCp1is required for myonuclear clustering in mid, while autophagy contributes to central positioning of nuclei in late metamorphosis. In conclusion, studying muscle remodelling in metamorphosis can provide new insights into the cell biology of muscle wasting.