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Cell Host Microbe. 2017 Sep 13;22(3):302-316.e7. doi: 10.1016/j.chom.2017.07.020. Epub 2017 Aug 31.

Legionella pneumophila Modulates Mitochondrial Dynamics to Trigger Metabolic Repurposing of Infected Macrophages.

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Institut Pasteur, Biologie des Bactéries Intracellulaires, Paris 75724, France; CNRS UMR 3525, Paris 75724, France.
Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019 - UMR 8204-CIIL-Center for Infection and Immunity of Lille, 59000 Lille, France.
Institute of Medical Microbiology, University of Zurich, Zurich, Switzerland.
Institut Pasteur, Unité d'Analyse d'Images Biologiques, CNRS UMR 3691, Paris, France.
VIB-UGent Center for Medical Biotechnology, Ghent University, 9000 Ghent, Belgium; VIB Proteomics Core, Ghent University, 9000 Ghent, Belgium; Department of Biochemistry, Ghent University, 9000 Ghent, Belgium.
Institut Pasteur, Biologie des Bactéries Intracellulaires, Paris 75724, France; CNRS UMR 3525, Paris 75724, France. Electronic address:


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.


DNM1L; Legionella pneumophila; bioenergetics; host-pathogen interactions; live cell imaging; mitochondrial dynamics; virulence

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