Lipid Droplets Guard Mitochondria during Autophagy Till Klecker, Ralf J. Braun, Benedikt Westermann  Developmental Cell  Volume 42, Issue 1, Pages 1-2 (July 2017) DOI: 10.1016/j.devcel.2017.06.018 Copyright © 2017 Elsevier Inc. Terms and Conditions

Figure 1 Avoiding Lipotoxicity: Fatty Acids Are Forced to Make a Pit Stop in Lipid Droplets on Their Way from Autophagosomes to Mitochondria In starved cells, fatty acids (FAs) are released during the autophagic degradation of membranous organelles. Instead of being directly transported to mitochondria for energy generation by β oxidation, FAs are rerouted to the ER, where they are used by diacylglycerol acyltransferase 1 (DGAT1) to synthesize triacylglycerols (TAGs), which are stored in ER-derived lipid droplets (LDs). At the same time, TAG stores within LDs are used by the lipolytic enzyme adipose triglyceride lipase (ATGL) to generate FAs. These are subsequently converted to acylcarnitine (AC) by carnitine palmitoyltransferase 1 (CPT1) and transported into mitochondria, where they fuel ATP production by β oxidation. ACs pose a major threat to the cell because they can damage mitochondria, resulting in mitochondrial dysfunction. Strikingly, LDs and mitochondria are frequently found in close proximity, most likely because they form contact sites to facilitate efficient FA transport. The molecular constituents of the tethering complex that juxtaposes LDs and mitochondria are currently unknown. Developmental Cell 2017 42, 1-2DOI: (10.1016/j.devcel.2017.06.018) Copyright © 2017 Elsevier Inc. Terms and Conditions