title: Functions and effectors of the Salmonella pathogenicity island 2 type III secretion system.
abstract: Salmonella enterica uses two functionally distinct type III secretion systems encoded on the pathogenicity islands SPI-1 and SPI-2 to transfer effector proteins into host cells. A major function of the SPI-1 secretion system is to enable bacterial invasion of epithelial cells and the principal role of SPI-2 is to facilitate the replication of intracellular bacteria within membrane-bound Salmonella-containing vacuoles (SCVs). Studies of mutant bacteria defective for SPI-2-dependent secretion have revealed a variety of functions that can be attributed to this secretion system. These include an inhibition of various aspects of endocytic trafficking, an avoidance of NADPH oxidase-dependent killing, the induction of a delayed apoptosis-like host cell death, the control of SCV membrane dynamics, the assembly of a meshwork of F-actin around the SCV, an accumulation of cholesterol around the SCV and interference with the localization of inducible nitric oxide synthase to the SCV. Several effector proteins that are translocated across the vacuolar membrane in a SPI-2-dependent manner have now been identified. These are encoded both within and outside SPI-2. The characteristics of these effectors, and their relationship to the physiological functions listed above, are the subject of this review. The emerging picture is of a multifunctional system, whose activities are explained in part by effectors that control interactions between the SCV and intracellular membrane compartments.
authors.affiliation: Hanson Institute, Institute of Medical and Veterinary Science, Adelaide, Australia.
authors.forename: Scott R
authors.initials: SR
authors.lastname: Waterman
authors.forename: David W
authors.initials: DW
authors.lastname: Holden
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D016923:Cell Death; D002784:Cholesterol / Q000378:metabolism; D006023:Glycoproteins / Q000235:genetics / Q000502:physiology; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics / Q000502:physiology*; D008954:Models, Biological; D009154:Mutation; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D016897:Respiratory Burst; D019779:Salmonella enterica / Q000235:genetics / Q000472:pathogenicity* / Q000502:physiology*; D014157:Transcription Factors / Q000235:genetics / Q000502:physiology; D014617:Vacuoles / Q000378:metabolism / Q000382:microbiology; D014774:Virulence / Q000235:genetics / Q000502:physiology
chemical_list: D000199:Actins; D001426:Bacterial Proteins; D006023:Glycoproteins; D008565:Membrane Proteins; C440638:SPI-2 protein, Salmonella; C421862:SifA protein, Salmonella; C120280:SpiC protein, Salmonella; C119761:SsrB protein, Salmonella typhimurium; D014157:Transcription Factors; D002784:Cholesterol; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II