The study investigates the regulation of autophagy termination and lysosome reformation by mTOR signaling during starvation. Autophagy, an essential process for catabolizing cytoplasmic components, is initiated by inhibiting the target of rapamycin (TOR), a nutrient-responsive kinase. During autophagy, autophagosomes form and fuse with lysosomes to degrade their contents. However, the fate of autolysosomes and subsequent lysosome homeostasis during prolonged starvation was not well understood. The authors found that mTOR signaling is inhibited during autophagy initiation but reactivated with prolonged starvation, which attenuates autophagy and triggers the formation of proto-lysosomal tubules and vesicles. These tubules and vesicles mature into functional lysosomes, restoring the full complement of lysosomes in the cell. This process, termed autophagic lysosome reformation (ALR), is regulated by mTOR and involves the dissociation of Rab7 from tubules. Genetic or chemical inhibition of lysosome function prevents ALR, suggesting that lysosomal degradative capability is crucial for this process. The study provides insights into the negative feedback mechanism that couples nutritional status to autophagy, ensuring nutrient replenishment prevents excess autophagy and potential autophagic cell death.The study investigates the regulation of autophagy termination and lysosome reformation by mTOR signaling during starvation. Autophagy, an essential process for catabolizing cytoplasmic components, is initiated by inhibiting the target of rapamycin (TOR), a nutrient-responsive kinase. During autophagy, autophagosomes form and fuse with lysosomes to degrade their contents. However, the fate of autolysosomes and subsequent lysosome homeostasis during prolonged starvation was not well understood. The authors found that mTOR signaling is inhibited during autophagy initiation but reactivated with prolonged starvation, which attenuates autophagy and triggers the formation of proto-lysosomal tubules and vesicles. These tubules and vesicles mature into functional lysosomes, restoring the full complement of lysosomes in the cell. This process, termed autophagic lysosome reformation (ALR), is regulated by mTOR and involves the dissociation of Rab7 from tubules. Genetic or chemical inhibition of lysosome function prevents ALR, suggesting that lysosomal degradative capability is crucial for this process. The study provides insights into the negative feedback mechanism that couples nutritional status to autophagy, ensuring nutrient replenishment prevents excess autophagy and potential autophagic cell death.