Toxoplasma gondii sequesters lysosomes from mammalian hosts in the vacuolar space

Cell 125, 261-274, 2006

Speaker：葉駿達                                                 Commentator：胥直利老師

Date：2006/06/07 15:10~16:00                          Place：Room 601

Abstract：

Toxoplasma gondii, a common intracellular pathogen, is adapted to thrive in a unique, self-made parasitophorous vacuole (PV) within the cytoplasm of a large variety of mammalian cells. It is still unclear how T. gondii acquires nutrients from the host cell without intersecting the host cell endocytic pathway. The authors observed some mechanisms that led to the sequestration of materials from the host endocytic compartments to T. gondii. The parasite can recruit host microtubules (MT) actively to attract the endo-lysosome to PV. MT-based invaginations of the parasitophorous vacuole membrane (PVM) serve as conduits for the transport of host organelles into the vacuolar space. Also, they found these conduits are stabilized by the secreted parasite coat proteins, e.g. GRA7, which act like a garrote that sequesters host endocytic organelles in the vacuolar space, resulting in PVM constriction and hence sequestration of host endo-lysosome. The intralysosomal molecules produced by hydrolysis can cross the lysosome membrane via carrier-mediated transporters and can be translocated across the parasite plasma membrane. The authors argued that their findings identify a unique mechanism for unidirectional transport and sequestration of host organelles.

References：

(1) Coppens, I., and Joiner, K.A. (2003). Host but not parasite cholesterol controls Toxoplasma cell entry by modulating organelle discharge. Mol. Biol. Cell 14, 3804–3820.

(2) Coppens, I., Sinai, A.P., and Joiner, K.A. (2000). Toxoplasma gondii exploits host low-density lipoprotein receptor-mediated endocytosis for cholesterol acquisition. J. Cell Biol.149, 167–180.