Abstract
Autophagy is an evolutionarily conserved lysosome-based degradation process. Stimuli such as nutrients starvation induce formation of autophagosome, which then fuse with lysosome to form autolysosome. After degradation of engulfed cellular content, lysosomes are recycled from autolysosomes through an evolutionarily conserved process named autophagic lysosome reformation (ALR), which is triggered by reactivation of mTOR during prolonged starvation. Our previous study identified ASAP1, the GAP protein for ARF1, is a regulator of ALR. In this study, we report that ARF1 is translocated to autolysosome during ALR. Knocking down ASAP1, or overexpression GTP binding form of ARF1, can block the mTOR reactivation and ALR. Thus, ARF1 and ASAP1 regulate ALR through regulating mTOR reactivation.
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