2016
DOI: 10.1242/jcs.185223
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Apicoplast fatty acid synthesis is essential for pellicle formation at the end of cytokinesis in Toxoplasma gondii

Abstract: The apicomplexan protozoan Toxoplasma gondii, the causative agent of toxoplasmosis, harbors an apicoplast, a plastid-like organelle with essential metabolic functions. Although the FASII fatty acid biosynthesis pathway located in the apicoplast is essential for parasite survival, the cellular effects of FASII disruption in T. gondii had not been examined in detail. Here, we combined light and electron microscopy techniques -including focused ion beam scanning electron microscopy (FIB-SEM) -to characterize the … Show more

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Cited by 35 publications
(25 citation statements)
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“…Second, Tg AP1 could be involved in a recycling activity of the mother plasma membrane from the residual body to terminate daughter cell segregation, such as previously observed for the IMC [62] or contribute to a direct transport of de novo synthesized lipids from the TGN to the plasma membrane. In agreement with the latter hypothesis, a recent study has demonstrated that parasite depleted for the FAS II enzyme, which is responsible for fatty acid biosynthesis at the apicoplast, displayed drastic division defects and were unable to segregate after the budding process has completed, forming a mass of tethered cells [63]. This study revealed the requirement for de novo lipid synthesis and therefore, we believe, of regulated trafficking pathways for the delivery of these lipids, to complete daughter cell segregation at the end of cytokinesis.…”
Section: Discussionmentioning
confidence: 66%
“…Second, Tg AP1 could be involved in a recycling activity of the mother plasma membrane from the residual body to terminate daughter cell segregation, such as previously observed for the IMC [62] or contribute to a direct transport of de novo synthesized lipids from the TGN to the plasma membrane. In agreement with the latter hypothesis, a recent study has demonstrated that parasite depleted for the FAS II enzyme, which is responsible for fatty acid biosynthesis at the apicoplast, displayed drastic division defects and were unable to segregate after the budding process has completed, forming a mass of tethered cells [63]. This study revealed the requirement for de novo lipid synthesis and therefore, we believe, of regulated trafficking pathways for the delivery of these lipids, to complete daughter cell segregation at the end of cytokinesis.…”
Section: Discussionmentioning
confidence: 66%
“…In mammalian cells, cellular fatty acid homeostasis reflects an equilibrium between production processes (e.g., de novo synthetic pathways and hydrolysis of TAG/phospholipids by lipases and import) and utilization processes (e.g., for membrane biosynthesis, energy production through ␤-oxidation, generation of lipid signaling molecules, posttranslational protein modification, and transcriptional regulation) (63). Fatty acid metabolism in Toxoplasma consists of both synthetic and salvaging pathways (64)(65)(66). The parasite can synthesize several major fatty acids through three pathways: cytosolic fatty acid synthetic pathway I (FASI); a unique FASII pathway located in the plastid-like organelle, termed the apicoplast; and the fatty acid elongation system in the ER (66).…”
Section: Discussionmentioning
confidence: 99%
“…Fatty acid metabolism in Toxoplasma consists of both synthetic and salvaging pathways (64)(65)(66). The parasite can synthesize several major fatty acids through three pathways: cytosolic fatty acid synthetic pathway I (FASI); a unique FASII pathway located in the plastid-like organelle, termed the apicoplast; and the fatty acid elongation system in the ER (66). Pharmacological interference with FASII prevents the completion of parasite cytokinesis; however, supplementation with FASII products, e.g., myristate, PA, or OA, can rescue the cytokinesis defect, which highlights the importance of fatty acid salvage pathways in Toxoplasma (18).…”
Section: Discussionmentioning
confidence: 99%
“…How parasites are able to compensate for this loss during the first lytic cycle remains poorly understood. Of note, growth kinetics resembling delayed death have also been observed for inhibitors that block apicoplast metabolic function and genetic disruption of proteins required for apicoplast biogenesis or metabolism, suggesting that inhibiting production of essential apicoplast metabolites may be the common perturbation leading to delayed death in T. gondii (5, 1518).…”
Section: Introductionmentioning
confidence: 96%