Genes controlling muscle size and survival play important roles in muscle wasting diseases. In
Drosophila melanogaster
metamorphosis, 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 of
in vivo
imaging, targeted gene perturbation and quantitative image analysis. We show that inhibition of
TOR
signalling and activation of autophagy promote developmental muscle atrophy in early, while
TOR
and
yorkie
activation 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 orthologue
Cp1
is 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.