Figure 1. SseL deubiquitinates cytosolic aggregates destined for autophagy. In the presence of SseL, both ALIS, and aggregates that form in response to S. Typhimurium SPI-2 T3SS effectors, are deubiquitinated. The fate of deubiquitinated cytosolic aggregates is not known. In the absence of SseL, ALIS and SPI-2 T3SS-induced aggregates are ubiquitinated and recruit SQSTM1 and LC3. This leads to engulfment of aggregates by autophagic membranes and their subsequent degradation in lysosomes. Abbreviations: LPS; lipopolysaccharide; Ub, ubiquitin; ALIS, aggresome-like induced structure; TLR, toll-like receptor; SseL, S. Typhimurium secreted effector L; SPI-2, S. Typhimurium pathogenicity island 2; SQSTM1, sequestosome 1; T3SS, Type III secretion system.