Journal
CELL HOST & MICROBE
Volume 22, Issue 3, Pages 302-+Publisher
CELL PRESS
DOI: 10.1016/j.chom.2017.07.020
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Funding
- Institut Pasteur
- ANR [ANR-10-LABX-62-IBEID, ANR-13-IFEC-0003-02, ANR-10-INSB-04-01, ANR-10-EQPX-04-01]
- ANR (Infect-ERA project EUGENPATH)
- Fondation pour la Recherche Medicale (FRM) [DEQ20120323697]
- Conseil de la Region Ile-de-France, FRM
- Technology Core of the Center for Translational Science (CRT) at Institut Pasteur
- Roux Fellowship (Institut Pasteur)
- Institute of Medical Microbiology, University of Zurich
- Swiss National Science Foundation (SNF) [31003A_153200]
- German Bundesministerium fur Bildung und Forschung (BMBF) [031A410A]
- VIB
- Research Foundation Flanders (FWO) [G0F8616N]
- European Community [260901, 260872]
- Region Nord Pas de Calais [12000080]
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The intracellular bacteria Legionella pneumophila encodes a type IV secretion system (T4SS) that injects effector proteins into macrophages in order to establish and replicate within the Legionella-containing vacuole (LCV). Once generated, the LCV interacts with mitochondria through unclear mechanisms. We show that Legionella uses both T4SS-independent and T4SS-dependent mechanisms to respectively interact with mitochondria and induce mitochondrial fragmentation that ultimately alters mitochondrial metabolism. The T4SS effector MitF, a Ran GTPase activator, is required for fission of the mitochondrial network. These effects of MitF occur through accumulation of mitochondrial DNM1L, a GTPase critical for fission. Furthermore mitochondrial respiration is abruptly halted in a T4SS-dependent manner, while T4SS-independent upregulation of cellular glycolysis remains elevated. Collectively, these alterations in mitochondrial dynamics promote a Warburg-like phenotype in macrophages that favors bacterial replication. Hence the rewiring of cellular bioenergetics to create a replication permissive niche in host cells is a virulence strategy of L. pneumophila.
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