title: How cells deploy ubiquitin and autophagy to defend their cytosol from bacterial invasion.
abstract: Autophagy serves as a cell-autonomous effector mechanism of innate immunity in the cytosol. Autophagy restricts bacterial proliferation by separating bacteria from the nutrient-rich cytosol and delivering them into bactericidal autolysosomes. Autophagy also restricts inflammation by enclosing the membrane remnants of vacuoles from which bacteria have escaped. In contrast to starvation-induced autophagy, which engulfs cytosol nonspecifically, antibacterial autophagy is receptor-mediated and selective. Several distinct pathways of antibacterial autophagy have been identified recently, which can be triggered by either bacterial PAMPs, host-mediated modifications of bacteria-containing vacuoles, or cytosolic bacteria that have become decorated with ubiquitin. Ubiquitin-coated bacteria are sensed by p62, a promiscuous autophagy receptor required for the uptake of a variety of ubiquitin-marked autophagy substrates, and by NDP52, an autophagy receptor that, by associating with the immunoregulatory kinase TBK1, may serve a dedicated function in cytosolic immunity.
authors.affiliation: MRC Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Cambridge, UK. randow@mrc-lmb.cam.ac.uk
authors.forename: Felix
authors.initials: F
authors.lastname: Randow
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000737:chemistry / Q000378:metabolism; D000818:Animals; D001343:Autophagy; D001419:Bacteria / Q000378:metabolism*; D003600:Cytosol / Q000276:immunology / Q000382:microbiology*; D006801:Humans; D008954:Models, Biological; D025801:Ubiquitin / Q000378:metabolism*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D025801:Ubiquitin