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Bacterial Pathogens Commandeer Rab GTPases to Establish Intracellular Niches
Author(s) -
Stein MaryPat,
Müller Matthias P.,
WandingerNess Angela
Publication year - 2012
Publication title -
traffic
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.677
H-Index - 130
eISSN - 1600-0854
pISSN - 1398-9219
DOI - 10.1111/tra.12000
Subject(s) - rab , biology , microbiology and biotechnology , gtpase , effector , legionella pneumophila , intracellular parasite , endosome , intracellular , endocytic cycle , endocytosis , biochemistry , cell , bacteria , genetics
Intracellular bacterial pathogens deploy virulence factors termed effectors to inhibit degradation by host cells and to establish intracellular niches where growth and differentiation take place. Here, we describe mechanisms by which human bacterial pathogens (including Chlamydiae; Coxiella burnetii; Helicobacter pylori; Legionella pneumophila; Listeria monocytogenes; Mycobacteria; Pseudomonas aeruginosa, Salmonella enterica) modulate endocytic and exocytic Rab GTPases in order to thrive in host cells. Host cell Rab GTPases are critical for intracellular transport following pathogen phagocytosis or endocytosis. At the molecular level bacterial effectors hijack Rab protein function to: evade degradation, direct transport to particular intracellular locations and monopolize host vesicles carrying molecules that are needed for a stable niche and/or bacterial growth and differentiation. Bacterial effectors may serve as specific receptors for Rab GTPases or as enzymes that post-translationally modify Rab proteins or endosomal membrane lipids required for Rab function. Emerging data indicate that bacterial effector expression is temporally and spatially regulated and multiple virulence factors may act concertedly to usurp Rab GTPase function, alter signaling and ensure niche establishment and intracellular bacterial growth, making this field an exciting area for further study.