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. 2018 Mar 24;18(4):foy034. doi: 10.1093/femsyr/foy034

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© FEMS 2018.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — Perspectives view of how lipid traffic could affect cellular lipotoxicity. Externally supplied lipids such as palmitoleic acid (POA) and dioctanoyl glycerol (DOG) trigger necrosis in yeast. Here, we schematically depict the potential cellular lipid trafficking routes and potential involvement of vesicular and MCS-mediated transport. Lipids can be internalised by endocytosis, direct interaction with PM-lipids or receptor/translocase-mediated (not shown) pathways. Once internalised, lipids may be transported via the vesicular ESCRT-dependent trafficking route or via contact sites. Lipid-containing endosomes can interact and exchange lipids with the ER and/or LD, which could further deliver lipids to other organelles including the vacuole, mitochondria and Golgi via fusion events or lipid exchange through MCS. Lipids can trigger ER stress and potentially disrupt ER-membrane integrity. In order to alleviate from ER-stress/toxicity, toxic lipids could be channelled into the Golgi, mitochondria and LDs for metabolisation or storage purposes. LDs can remobilise stored lipids via lipolysis or lipophagy. Delivery of external-lipid-containing-endosomes can fuse with the vacuole possibly involving HOPS/CORVET or other SNARE/Rab machineries. Toxic lipids could then be delivered to the PM via recycling endosomes and thus disrupt PM integrity. Toxic lipids reaching the mitochondria could induce MOMP and thus induce cell death via mitochondrial pathways.