Figure 3

Figure 3

Host-protective and host-detrimental interactions of bacterial pathogens with the autophagy machinery in zebrafish infection models. (A) p62-dependent xenophagy restricts growth of S. flexneri bacteria in macrophages of the zebrafish host. (B) In the zebrafish M. marinum model, p62, Optn, and Dram1 are required for host resistance. p62 and Optn both mediate xenophagy in infected macrophages, while Dram1, an integral membrane protein of intracellular vesicles including lysosomes, promotes vesicle fusion events. (C) LAP, which requires the signaling molecule Rubicon (Rubcn) and the Cyba component of NADPH oxidase, is the predominant defense response of zebrafish macrophages to S. Typhimurium infection. (D) In zebrafish neutrophils, Cyba-mediated LAP provides a replication niche for S. aureus, while p62-mediated xenophagy counteracts the growth of bacteria that may be released from phagosomes or LAPosomes. Functions of the proteins indicated in bold have been demonstrated by knockdown, mutation, and/or overexpression analyses. See the text for references.