Model for a role of Dyn2 in autophagic breakdown of lipid droplets in hepatocytes. After initiation of starvation, lipid droplets are enclosed by the double-membrane isolation membrane (phagophore), which engulfs the droplet, forming an autophagosome. Subsequent fusion with lysosomes results in the release of hydrolytic enzymes and lysosomal lipases into the autolysosomal compartment, which degrade the lipid droplets within. During the process of autophagic lysosomal reformation (top), nascent lysosomes are generated from membrane tubule extensions of this autolysosomal compartment. Dyn2 mediates the scission of these tubular structures. Depletion of Dyn2 by siRNA knockdown or inhibition of Dyn2 activity by pharmacological reagents (bottom) prevents tubular scission, eventually resulting in depleted lysosomal pools within the cell. Continued fusion of remaining lysosomes causes enlargement of the autolysosomal structures. A complete decrease in the recycled lysosomal population will prevent autophagic-mediated breakdown of hepatic lipid droplets.