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Intracellular growth of Toxoplasma gondii requires association with respiration‐competent mitochondria
Author(s) -
Andrews Joel F,
Barik Sailen
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.510.1
Subject(s) - mitochondrion , toxoplasma gondii , microbiology and biotechnology , intracellular , organelle , intracellular parasite , dynein , biology , vacuole , microtubule , chemistry , cytoplasm , immunology , antibody
Toxoplasma gondii ( Tg ) is an intracellular parasite that causes the disease toxoplasmosis. Tg grows within a parasitophorous vacuole (PV), a parasite‐modified space surrounded by the parasitophorous vacuolar membrane (PVM), to which host mitochondria and other organelles are recruited. It is our objective to characterize the mechanism and significance of mitochondrial association with the PVM (mito‐PVM association). Initial studies showed that mito‐PVM association is microtubule‐dependent. Using chemical inhibitors, protein over‐expression constructs, and siRNA we have shown that microtubule‐dependent mito‐PVM association requires a functional host dynein/dynactin complex. Tg growth is reduced when mito‐PVM association is inhibited. Tg scavenges lipids from mitochondria, but the significance of host mitochondrial ATP production for Tg is unknown. To address mitochondrial ATP production, a cell line defective in mitochondrial respiration was infected with Tg tachyzoites. Tg growth, development, and egress were significantly inhibited in the respiration‐defective cell line, despite no difference in mito‐PVM association or cellular ATP levels. These results suggest that Tg growth is dependent on association with aerobically respiring mitochondria. Supported by Alabama EPSCoR and NIH Grant A1059267