ausblenden:
Schlagwörter:
Animals
Cell Line
GTP Phosphohydrolases/metabolism
Humans
Intracellular Membranes/physiology/ultrastructure
Mice
Mitochondrial Membrane Transport Proteins/metabolism
Mitochondrial Membranes/*physiology/ultrastructure
Mitochondrial Precursor Protein Import Complex Proteins/*metabolism
Mitochondrial Proteins/metabolism
Protein Binding
Protozoan Proteins/*metabolism
Stress, Physiological
Toxoplasma/growth & development/*physiology/ultrastructure
Toxoplasmosis/parasitology
Vacuoles/physiology/ultrastructure
Zusammenfassung:
The outer mitochondrial membrane (OMM) is essential for cellular homeostasis. Yet little is known of the mechanisms that remodel it during natural stresses. We found that large "SPOTs" (structures positive for OMM) emerge during Toxoplasma gondii infection in mammalian cells. SPOTs mediated the depletion of the OMM proteins mitofusin 1 and 2, which restrict parasite growth. The formation of SPOTs depended on the parasite effector TgMAF1 and the host mitochondrial import receptor TOM70, which is required for optimal parasite proliferation. TOM70 enabled TgMAF1 to interact with the host OMM translocase SAM50. The ablation of SAM50 or the overexpression of an OMM-targeted protein promoted OMM remodeling independently of infection. Thus, Toxoplasma hijacks the formation of SPOTs, a cellular response to OMM stress, to promote its growth.
