Autophagy is a conserved process that degrades cytoplasmic proteins and organelles during starvation. The target of rapamycin (mTOR) is inhibited during starvation, inducing autophagy. Autophagosomes engulf cellular components and fuse with lysosomes to form autolysosomes, which degrade their contents. However, the regulation of autophagy in response to nutrients and the fate of autolysosomes remain unclear. This study shows that mTOR signaling is inhibited during autophagy initiation but reactivated with prolonged starvation. mTOR reactivation is autophagy-dependent and requires the degradation of autolysosomal products. Increased mTOR activity attenuates autophagy and generates protolysosomal tubules and vesicles that extrude from autolysosomes and mature into functional lysosomes, restoring lysosome homeostasis. During starvation, lysosomes fuse with autophagosomes, leading to the formation of larger autolysosomes. However, after 12 hours of starvation, lysosome size and number recover, indicating a homeostatic cycle involving the consumption and restoration of lysosomes during autophagy. Lysosome reformation occurs through the formation of tubules and vesicles that extrude from autolysosomes. These tubules and vesicles lack key biochemical characteristics of autolysosomes or lysosomes but eventually mature into functional lysosomes. This process is regulated by mTOR signaling, which is reactivated during prolonged starvation. mTOR reactivation inhibits autophagy and stimulates the recycling of lysosomal membrane components. The study also shows that mTOR is activated by growth factors and nutrients, and that autophagy provides nutrients by degrading cellular contents. The study further demonstrates that mTOR reactivation is triggered by the degradation of autolysosomal products, which in turn inhibits autophagy and initiates lysosome reformation. This negative feedback mechanism ensures that autophagy is self-regulated, preventing excessive autophagy that could lead to autophagic cell death. The study provides evidence that lysosomal degradative capability is required for lysosome reformation. The findings highlight the importance of mTOR signaling in regulating autophagy and lysosome homeostasis during starvation.Autophagy is a conserved process that degrades cytoplasmic proteins and organelles during starvation. The target of rapamycin (mTOR) is inhibited during starvation, inducing autophagy. Autophagosomes engulf cellular components and fuse with lysosomes to form autolysosomes, which degrade their contents. However, the regulation of autophagy in response to nutrients and the fate of autolysosomes remain unclear. This study shows that mTOR signaling is inhibited during autophagy initiation but reactivated with prolonged starvation. mTOR reactivation is autophagy-dependent and requires the degradation of autolysosomal products. Increased mTOR activity attenuates autophagy and generates protolysosomal tubules and vesicles that extrude from autolysosomes and mature into functional lysosomes, restoring lysosome homeostasis. During starvation, lysosomes fuse with autophagosomes, leading to the formation of larger autolysosomes. However, after 12 hours of starvation, lysosome size and number recover, indicating a homeostatic cycle involving the consumption and restoration of lysosomes during autophagy. Lysosome reformation occurs through the formation of tubules and vesicles that extrude from autolysosomes. These tubules and vesicles lack key biochemical characteristics of autolysosomes or lysosomes but eventually mature into functional lysosomes. This process is regulated by mTOR signaling, which is reactivated during prolonged starvation. mTOR reactivation inhibits autophagy and stimulates the recycling of lysosomal membrane components. The study also shows that mTOR is activated by growth factors and nutrients, and that autophagy provides nutrients by degrading cellular contents. The study further demonstrates that mTOR reactivation is triggered by the degradation of autolysosomal products, which in turn inhibits autophagy and initiates lysosome reformation. This negative feedback mechanism ensures that autophagy is self-regulated, preventing excessive autophagy that could lead to autophagic cell death. The study provides evidence that lysosomal degradative capability is required for lysosome reformation. The findings highlight the importance of mTOR signaling in regulating autophagy and lysosome homeostasis during starvation.