Abstract
Author SummaryRecent discoveries have revealed the remarkable functional diversity of mitochondria in roles other than energy production, including an integral role for mitochondria and their dynamics in the regulation of the innate immune response. Interestingly, host mitochondria are recruited to the membranes that surround certain intracellular bacteria and parasites during infection. To date, how and why this phenomenon occurs has been a mystery, although it has been proposed to provide a metabolic benefit to the microbes. Here we identify mitochondrial association factor 1 (MAF1) as the parasite protein that mediates the association between the protozoan pathogen Toxoplasma and host mitochondria during infection. We show that MAF1 is needed to recruit host mitochondria to the Toxoplasma-containing vacuole and that this process is associated with changes in the immune response in infected cells and animals. These findings show that recruitment and association with host mitochondria is an important means by which intracellular pathogens interface with their host. We also find that the cost–benefit outcome of altering mitochondrial function might differ between strains depending on the precise niche in which they evolved; for infectious agents, these differences likely reflect different host organisms.
Highlights
Mitochondria are highly dynamic organelles that, besides producing energy and regulating apoptotic and Ca2+ signals, play a key role in orchestrating several aspects of cell function and behavior including autophagy, apoptosis, and immune signaling [1,2,3]
Host mitochondria are recruited to the membranes that surround certain intracellular bacteria and parasites during infection
We identify mitochondrial association factor 1 (MAF1) as the parasite protein that mediates the association between the protozoan pathogen Toxoplasma and host mitochondria during infection
Summary
Mitochondria are highly dynamic organelles that, besides producing energy and regulating apoptotic and Ca2+ signals, play a key role in orchestrating several aspects of cell function and behavior including autophagy, apoptosis, and immune signaling [1,2,3]. Recent evidence indicates that mitochondrial dynamics, including distribution, size, and shape, are linked to altered regulation of certain innate immune responses [4,5] Given this diversity of function, it is no surprise that mitochondria have recently emerged as central to host–pathogen interactions, with an increasing number of viruses and bacteria having been shown to manipulate host mitochondria in their roles in apoptosis, energy production, and immune function. Production [6], and Helicobacter pylori vacuolating cytotoxin (VacA) engages the machinery involved in regulation of mitochondrial fission to induce apoptosis [7] In light of these newly established roles for mitochondria and their targeting by different microbial effector proteins, it is interesting that during infection with certain pathogens host mitochondria associate with and appear sequestered at the vacuole in which the microbes reside. In the case of T. gondii, three predominant, clonal lineages have been
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