FIG 8.
Working model. In the feeding state, ATGL-1 is actively degraded by the proteasome pathway to maintain a low rate of basal lipolysis. In the fasting state, increased cAMP levels activate PKA signaling. Then, PKA phosphorylates and stabilizes ATGL-1, which is recruited to lipid droplets via interaction with LID-1, eventually stimulating lipid hydrolysis.