Journal
BIOESSAYS
Volume 39, Issue 2, Pages -Publisher
WILEY
DOI: 10.1002/bies.201600171
Keywords
autophagy; Legionella pneumophila; mitochondria; mitochondria-associated ER membranes
Categories
Funding
- French Region Ile de France (DIM Malinf)
- Infect-ERA project EUGENPATH [ANR-13-IFEC-0003-02]
- Fondation pour la Recherche Medicale grant [DEQ20120323697]
- Institut Pasteur
- [ANR-10-LABX-62-IBEID]
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Pathogenic bacteria frequently target the endoplasmic reticulum (ER) and mitochondria in order to exploit host functions. ER-mitochondria inter-organelle communication is topologically sub-compartmentalized at mitochondriaassociated ER membranes (MAMs). MAMs are specific membranous microdomains with unique regulatory functions such as lipid synthesis and trafficking, calcium homeostasis, mitochondrial morphology, inflammasome activation, autophagosome formation, and apoptosis. These important cellular processes are all modulated by pathogens to subvert host functions and promote infection, thus it is tempting to assume that pathogenic bacteria target MAMs to subvert these different pathways in their hosts. First lines of evidence that support this hypothesis come from Legionella pneumophila. This intracellular bacterium secretes an effector that exhibits sphingosine-1 phosphate lyase activity (LpSpl) that seems to target MAMs to modulate the autophagy response to infection. Here we thus propose the concept that MAMs could be targeted by pathogenic bacteria to undermine key host cellular processes.
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