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. 2021 May 17;12:2813. doi: 10.1038/s41467-021-22956-w

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Schematic representation of the dual essential role of TgLIPIN in parasite lipid metabolism, including, membrane biogenesis, and lipid storage. a The parasite utilizes, and glycerol-3-phosphate (G-3-P) and fatty acid (FA)s derived from both apicoplast (Api) FASII and host to synthesize major lipids by forming lysophosphatidic acid (LPA) followed by phosphatidic acid (PA). PA is hydrolyzed by TgLIPIN to generate diacylglycerol (DAG), which is further acylated to generate triacylglycerol (TAG). The other branch of this pathway redirects PA toward the generation of major membrane phospholipids. The FA homeostasis between membrane biogenesis and storage essential for normal parasite development within its host is maintained by the PA phosphatase TgLIPIN. b Genetic ablation of TgLIPIN in TgLIPIN-ikD parasites in the presence of anhydrotetracycline (ATc) caused the PA/DAG imbalance. The increased PA is channeled towards PL synthesis resulting in excess PLS and consequent gross membrane anomalies within the parasite IMC, nucleus, and ER, while forming giant multivesicular bodies (gMVBs). Simultaneously, the reduction in DAG affected TAG biogenesis and hence the lipid storage capacity, marked by decreased lipid droplets (LD), within the parasite lacking TgLIPIN. The impairment of TAG biosynthesis, resulted in excess fatty acids derived from the host, within TgLIPIN mutant, causing lipotoxicity.