Format

Send to

Choose Destination
Trends Microbiol. 2016 Jun;24(6):450-462. doi: 10.1016/j.tim.2016.02.003. Epub 2016 Feb 26.

Subversion of Retrograde Trafficking by Translocated Pathogen Effectors.

Author information

1
Institute of Medical Microbiology, Department of Medicine, University of Zürich, Gloriastrasse 30/32, 8006 Zürich, Switzerland.
2
Max von Pettenkofer Institute, Ludwig-Maximilians University Munich, Pettenkoferstrasse 9a, 80336 Munich, Germany.
3
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.

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.

KEYWORDS:

bacterial effector protein; host–pathogen interaction; pathogen vacuole; phosphoinositide lipid; retromer; small GTPase

PMID:
26924068
DOI:
10.1016/j.tim.2016.02.003
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center