Mitochondria Restrict Growth of the Intracellular Parasite Toxoplasma gondii by Limiting Its Uptake of Fatty Acids

Publication date: 3 April 2018
Source:Cell Metabolism, Volume 27, Issue 4
Author(s): Lena Pernas, Camilla Bean, John C. Boothroyd, Luca Scorrano
How intracellular pathogens acquire essential non-diffusible host metabolites and whether the host cell counteracts the siphoning of these nutrients by its invaders are open questions. Here we show that host mitochondria fuse during infection by the intracellular parasite Toxoplasma gondii to limit its uptake of fatty acids (FAs). A combination of genetics and imaging of FA trafficking indicates that Toxoplasma infection triggers lipophagy, the autophagy of host lipid droplets (LDs), to secure cellular FAs essential for its proliferation. Indeed, Toxoplasma FA siphoning and growth are reduced in host cells genetically deficient for autophagy or triglyceride depots. Conversely, Toxoplasma FA uptake and proliferation are increased in host cells lacking mitochondrial fusion, required for efficient mitochondrial FA oxidation, or where mitochondrial FA oxidation is pharmacologically inhibited. Thus, mitochondrial fusion can be regarded as a cellular defense mechanism against intracellular parasites, by limiting Toxoplasma access to host nutrients liberated by lipophagy.

Graphical abstract

Teaser

Intracellular microbes harness essential metabolites from the host cell. In this issue, Pernas et al. show that mitochondria mount a metabolic defense against the intracellular parasite Toxoplasma gondii by fusing around its vacuole and siphoning fatty acids that Toxoplasma liberates by activating autophagy of host lipid droplets.


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