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Toxoplasma Lipids Research Article 3049 Host cells: mobilizable lipid resources for the intracellular parasite Toxoplasma gondii Audra J. Charron and L. David Sibley* Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO 63110, USA *Author for correspondence (e-mail: [email protected]) Accepted 17 May 2002 Journal of Cell Science 115, 3049-3059 (2002) © The Company of Biologists Ltd Summary Successful replication of the intracellular parasite scavenged long-chain fatty acids as well as cholesterol, and Toxoplasma gondii within its parasitophorous vacuole in certain cases modified the host-derived lipids. When necessitates a substantial increase in membrane mass. The provided with radiolabeled phospholipid precursors, possible diversion and metabolism of host cell lipids and including polar head groups, phosphatidic acid and small lipid precursors by Toxoplasma was therefore investigated fatty acids, intracellular parasites preferentially accrued using radioisotopic and fluorophore-conjugated phosphatidylcholine (PtdCho) over other phospholipids. compounds. Confocal microscopic analyses demonstrated Moreover, Toxoplasma was found to be competent to that Toxoplasma is selective with regards to both the synthesize PtdCho from radiolabeled precursors obtained acquisition and compartmentalization of host cell from its environment. Together, these studies underscore lipids. Lipids were compartmentalized into parasite the ability of Toxoplasma gondii to divert and use lipid endomembranes and, in some cases, were apparently resources from its host, a process that may contribute to integrated into the surrounding vacuolar membrane. the biogenesis of parasite membranes. Additionally, some labels became concentrated in discrete lipid bodies that were biochemically and morphologically Key words: Cholesterol, Endocytosis, Exocytosis, Fatty acid, distinct from the parasite apical secretory organelles. Thin Organelle association, Parasitophorous vacuole, Phospholipid, layer chromatography established that parasites readily Phosphatidylcholine, Vesicular transport Introduction which are probably instrumental in the acquisition of host cell Eukaryotic cells invaded by Toxoplasma gondii acquire molecules (Carruthers and Sibley, 1997; Dubremetz et al., a unique and dynamic membranous organelle, the 1993). Throughout the extremely rapid course of invasion, host parasitophorous vacuole, the design of which accounts for the cell integral membrane proteins are largely excluded from the success of T. gondii as an intracellular pathogen. As the PVM (Mordue et al., 1999b). This exclusion results in the causative agent of human toxoplasmosis, this crescent-shaped formation of a membrane unique in its biochemical and protozoan is encompassed along with a variety of intracellular biophysical properties and the creation of a nonfusogenic parasites within the phylum Apicomplexa. Unified by a vacuole, securing parasites in a niche sequestered from host complex battery of apical organelles, apicomplexans cell endo/exocytic transport pathways (Mordue et al., 1999a; sequentially discharge these specialized organelles upon host Sibley et al., 1985). Ironically, the nonfusogenic PVM quickly cell invasion (Dubremetz et al., 1993). The initial attachment becomes physically associated with sites of host cell to host cells is mediated by the secretion of micronemes, which lipid biosynthesis, the endoplasmic reticulum (ER) and is succeeded immediately by the discharge of rhoptries mitochondrial membranes, a phenomenon that may be critical (Carruthers and Sibley, 1997). Rhoptry proteins are injected for the survival of the parasite (Endo et al., 1981; Jones et al., into the membranous indentation directly subjacent to the 1972; Sinai and Joiner, 2001; Sinai et al., 1997). These invading parasite, and several investigators have speculated coordinated events design an organelle poised for selective that rhoptries also contribute Toxoplasma lipids to the forming transactions with host cell organelles, which may facilitate the parasitophorous vacuole membrane (PVM) (Bannister et al., intracellular survival and growth of T. gondii. 1986; Foussard et al., 1991; Håkansson et al., 2001; Joiner, The inability of T. gondii to grow in vitro in the absence of 1991; Nichols et al., 1983). Concurrent with these processes, a host cell suggests that, in addition to protection from the parasite squeezes through a region of intimate membrane extracellular immune confrontations, its intracellular lifestyle apposition between the host and parasite termed the moving provides the parasite with some essential factor(s) unobtainable junction (Aikawa et al., 1977). The parasite is progressively in the extracellular milieu. The isolation from host cell translocated through the moving junction by its actinomyosin endo/exocytic pathways negates the possibility that the motor and it enters a compartment bounded by the PVM parasites require proteins or lipids whose trafficking is (Dobrowolski et al., 1997; Dobrowolski and Sibley, 1996). restricted to those pathways and suggests that the needed host Once established intracellularly, parasites extensively modify components are selectively mobilized via non-vesicular the PV by discharging their dense granules, the contents of transport routes. Candidate components include nucleobases, 3050 Journal of Cell Science 115 (15) amino acids, cytosolic proteins, and lipids. T. gondii is in fact phosphatidylcholine were prepared by combining either fluorescent auxotrophic for both purines and tryptophan (Pfefferkorn, cholesterol with unconjugated phosphatidylcholine (PtdCho) and 1984; Schwartzman and Pfefferkorn, 1982), and is afforded phosphatidylglycerol or fluorescent PtdCho with unconjugated access to small molecules (<1400 Da) via pores in the PVM cholesterol and phosphatidylglycerol to yield a final ratio of 1 (Schwab et al., 1994). In addition, low density lipoprotein cholesterol:0.9 PtdCho:0.1 phosphatidylglycerol. Lipid solutions (LDL)-complexed cholesterol is integrated into intracellular were combined in round-bottom flasks and immediately dried under a stream of argon with constant agitation with glass beads in a 40°C parasite membranes by an undefined mechanism (Coppens et water bath. After drying, the flask containing the lipid cake, al., 2000), indicating that T. gondii is competent to scavenge phosphate-buffered saline (PBS), and the glass beads was rapidly this lipid from its host. Because rapid parasite replication must rotated in a water bath sonicator set at 40°C. Liposomes were coincide with significant biogenesis of parasite membranes and collected and stored under argon at room temperature in glass vials. the concomitant enlargement of the PVM, it is plausible that Immediately prior to each use the liposomes were sonicated in a water parasites are adept at diverting and/or metabolizing host cell bath sonicator for 10 minutes at 37°C. Dried lipids and non-liposome membrane lipids or lipid precursors. This hypothesis was lipid solutions were stored dessicated at –20°C in single-use aliquots tested in the current study, which made use of fluorescent and until needed. The optimal dilution of each liposome and organic lipid radioactive lipid probes in conjunction with fluorescence solution was determined empirically for each experimental procedure. microscopy and thin layer chromatography. Cell culture Tachyzoites of the RH strain of T. gondii were maintained by serial Materials and Methods passage in human foreskin fibroblasts (HFFs) as previously described Reagents (Morisaki et al., 1995). HFFs and intracellular parasites were routinely The fluorescent lipid probes 5-butyl-4,4-difluoro-4-bora-3a,4a-diaza- cultured in D10 media (Dulbecco’s modified Eagle’s medium s-indacene-3-nonanoic acid (C4-BODIPY-C9), cholesteryl 4,4- containing 10% fetal bovine serum, 10 mM Hepes, 2 mM L- difluoro-5,7-dimethyl-4-bora-3a,4a-diaza-s-indacene-3-dodecanoate glutamine, and 2 µg/ml gentamycin). Mutant 89.1 cells and parental (cholesteryl BODIPY C12), 22-(N-(7-nitrobenz-2-oxa-1,3-diazol-4- CHO-K1 cells were cultured in H10 (Hams F12 media containing yl)amino)-23,24-bisnor-5-cholen-3β-ol (NBD-cholesterol), 2-(4,4- 10% fetal bovine serum, 10 mM Hepes, 2 mM L-glutamine, and 2 difluoro-5-(4-phenyl-1,3-butadienyl)-4-bora-3a,4a-diaza-s-indacene- µg/ml gentamycin). In preparation for experiments, host cells were 3-pentanoyl)-1-hexadecanoyl-sn-glycero-3-phosphocholine (BODI- grown to confluence in 12-well dishes or 100 mm diameter dishes or PY-phosphatidylcholine), 2-(4,4-difluoro-5,7-dimethyl-4-bora-3a, to near confluence on glass coverslips. 4a-diaza-s-indacene-3-pentanoyl)-1-hexadecanoyl-sn-glycero-3-phos- phate, diammonium salt (BODIPY-phosphatidic acid), and 4,4- Infection and labeling difluoro-5,7-dimethyl-4-bora-3a,4a-diaza-s-indacene-3-dodecanoic HFFs acid (BODIPY-C12) were obtained from Molecular Probes (Eugene, Host cells were washed with D10 in which lipid-containing serum was OR). Also from Molecular Probes were the far red-emitting nucleic substituted with delipidized bovine serum (DLS-D10). Rinsed cells acid dye TOPRO3 and the neutral lipid dye Nile red. All unlabeled were either prelabeled with lipids before parasite infection or lipids (cholesterol, L-α-phosphatidylcholine, phosphatidyl- preinfected with parasites before lipid labeling. In the first case, lipids ethanolamine, phosphatidylserine, phosphatidylinositol, phos- diluted in DLS-D10 were added to each well and the labeling phatidylglycerol, and sphingomyelin) were purchased from Avanti
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