Lipid droplets (LDs) are fat storage organelles that are central to lipid metabolism in cells. LDs interact with numerous other organelles, such as the endoplasmic reticulum (ER) and vacuoles. The latter uses autophagy-dependent mechanisms to mobilise fatty acids from LDs during starvation. However, the coordination of LD–organelle dynamics and the underlying metabolic network are poorly understood. In their Research Article (Ouahoud et al., 2018), Daniel Markgraf and colleagues employ a genome-wide screen in budding yeast coupled with flow cytometry to identify mutants in which LD consumption and dynamics are affected during growth resumption. They identified mutants in endosomal sorting complexes required for transport (ESCRT) and the vacuolar ATPase (V-ATPase) as having altered LD consumption, independent of autophagy. Specifically, ESCRT-mediated vacuole homeostasis is needed to enable the conversion of diacylglycerol (DAG) at LDs into phosphatidic acid (PA) and membrane lipids, and to mediate DAG channelling towards vacuoles through the target of rapamycin complex 1 (TORC1). Taken together, this study highlights the coupling of LD catabolism and TORC1 signalling from vacuoles during growth resumption to steer efficient utilisation of DAG for membrane lipid biosynthesis.