Manipulation of rab GTPase function by intracellular bacterial pathogens.
Intracellular bacterial pathogens have evolved highly specialized mechanisms to enter and survive within their eukaryotic hosts. In order to do this, bacterial pathogens need to avoid host cell degradation and obtain nutrients and biosynthetic precursors, as well as evade detection by the host immune system. To create an intracellular niche that is favorable for replication, some intracellular pathogens inhibit the maturation of the phagosome or exit the endocytic pathway by modifying the identity of their phagosome through the exploitation of host cell trafficking pathways. In eukaryotic cells, organelle identity is determined, in part, by the composition of active Rab GTPases on the membranes of each organelle. This review describes our current understanding of how selected bacterial pathogens regulate host trafficking pathways by the selective inclusion or retention of Rab GTPases on membranes of the vacuoles that they occupy in host cells during infection.
Cell Biology Program, The Hospital for sick Children, Toronto, Ontario M5G 1X8, Canada.
John H
JH
Brumell
Marci A
MA
Scidmore
D000818:Animals; D001419:Bacteria / Q000254:growth & development / Q000472:pathogenicity; D018407:Bacterial Physiological Phenomena; D002689:Chlamydia / Q000502:physiology; D016997:Coxiella burnetii / Q000502:physiology; D005057:Eukaryotic Cells / Q000378:metabolism / Q000382:microbiology; D016480:Helicobacter pylori / Q000502:physiology; D006801:Humans; D016952:Legionella pneumophila / Q000502:physiology; D009169:Mycobacterium tuberculosis / Q000502:physiology; D010588:Phagosomes / Q000382:microbiology / Q000502:physiology; D019779:Salmonella enterica / Q000502:physiology; D015398:Signal Transduction; D020691:rab GTP-Binding Proteins / Q000378:metabolism*
D020691:rab GTP-Binding Proteins