The mechanism for ERES uptake by autolysosome in Torin-treated cells. Under Torin treatment, ALG2 gets recruited to ERESs in response to increased cytosolic calcium. On one hand, ALG2 assists ubiquitination of the ERES COPII component, potentially increasing the association between ubiquitinated ERES and LC3 decorated autolysosomal membrane through autophagic receptors (i.e., p62). On the other hand, ALG2 recruited ALIX and ESCRT-III components, initiated membrane invagination on the autolysosomal membrane, and helped to engulf ERES components into autolysosomes.
