title: Phosphoinositide lipids and the Legionella pathogen vacuole.
abstract: Subversion of vesicle trafficking is vital for intracellular survival of Legionella pneumophila within host cells. L. pneumophila produces several type IV-translocated effector proteins that modify components of the phagosomal membrane, in particular the phosphoinositide (PI) lipids. Within eukaryotic cells PIs co-define subcellular compartments and membrane dynamics. The generation, half-life, and localization of PI lipids are not only tightly regulated by the host cell, but also targeted and modulated by a number of L. pneumophila effectors. These effectors either anchor to PIs, directly modify the lipids, or recruit PI-metabolizing enzymes to the LCV membrane. Together, PI-subverting L. pneumophila effectors act jointly to promote the formation of a replication-permissive niche inside the host.
authors.affiliation: Medical Faculty, Max von Pettenkofer Institute, Ludwig-Maximilians University, Munich Pettenkoferstrasse 9a, 80336, Munich, Germany.
authors.forename: Ina
authors.initials: I
authors.lastname: Haneburger
authors.forename: Hubert
authors.initials: H
authors.lastname: Hilbi
mesh_terms: D006801:Humans; D016952:Legionella pneumophila / Q000472:pathogenicity*; D008563:Membrane Lipids / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D010716:Phosphatidylinositols / Q000502:physiology*; D014617:Vacuoles / Q000382:microbiology*
chemical_list: D008563:Membrane Lipids; D010716:Phosphatidylinositols; D019869:Phosphatidylinositol 3-Kinases