title: Subversion of Retrograde Trafficking by Translocated Pathogen Effectors.
abstract: Intracellular bacterial pathogens subvert the endocytic bactericidal pathway to form specific replication-permissive compartments termed pathogen vacuoles or inclusions. To this end, the pathogens employ type III or type IV secretion systems, which translocate dozens, if not hundreds, of different effector proteins into their host cells, where they manipulate vesicle trafficking and signaling pathways in favor of the intruders. While the distinct cocktail of effectors defines the specific processes by which a pathogen vacuole is formed, the different pathogens commonly target certain vesicle trafficking routes, including the endocytic or secretory pathway. Recently, the retrograde transport pathway from endosomal compartments to the trans-Golgi network emerged as an important route affecting pathogen vacuole formation. Here, we review current insight into the host cell's retrograde trafficking pathway and how vacuolar pathogens of the genera Legionella, Coxiella, Salmonella, Chlamydia, and Simkania employ mechanistically distinct strategies to subvert this pathway, thus promoting intracellular survival and replication.
authors.affiliation: Institute of Medical Microbiology, Department of Medicine, University of Zürich, Gloriastrasse 30/32, 8006 Zürich, Switzerland.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Personnic
authors.affiliation: Institute of Medical Microbiology, Department of Medicine, University of Zürich, Gloriastrasse 30/32, 8006 Zürich, Switzerland.
authors.forename: Kevin
authors.initials: K
authors.lastname: Bärlocher
authors.affiliation: Max von Pettenkofer Institute, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9a, 80336 Munich, Germany.
authors.forename: Ivo
authors.initials: I
authors.lastname: Finsel
authors.affiliation: Institute of Medical Microbiology, Department of Medicine, University of Zürich, Gloriastrasse 30/32, 8006 Zürich, Switzerland; Max von Pettenkofer Institute, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9a, 80336 Munich, Germany. Electronic address: hilbi@imm.uzh.ch.
authors.forename: Hubert
authors.initials: H
authors.lastname: Hilbi
mesh_terms: D001426:Bacterial Proteins / Q000378:metabolism; D058947:Bacterial Secretion Systems / Q000502:physiology*; D002689:Chlamydia / Q000472:pathogenicity / Q000502:physiology; D002695:Chlamydiales / Q000472:pathogenicity / Q000502:physiology; D003381:Coxiella / Q000472:pathogenicity / Q000502:physiology; D004705:Endocytosis; D011992:Endosomes / Q000378:metabolism; D006056:Golgi Apparatus / Q000502:physiology; D054884:Host-Pathogen Interactions / Q000502:physiology*; D007875:Legionella / Q000472:pathogenicity / Q000502:physiology; D021381:Protein Transport / Q000502:physiology*; D012475:Salmonella / Q000472:pathogenicity / Q000502:physiology; D000069296:Type III Secretion Systems; D000069319:Type IV Secretion Systems; D014617:Vacuoles / Q000382:microbiology
chemical_list: D001426:Bacterial Proteins; D058947:Bacterial Secretion Systems; D000069296:Type III Secretion Systems; D000069319:Type IV Secretion Systems
keywords: bacterial effector protein; host–pathogen interaction; pathogen vacuole; phosphoinositide lipid; retromer; small GTPase