Aggregation of host endosomes by Salmonella requires SPI2 translocation of SseFG and involves SpvR and the fms–aroE intragenic region

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Abstract
Salmonella‐induced aggregation of host endosomal compartments into tubules, termed lgp‐tubules, requires sifA and ompR. Lgp‐tubules result from Salmonella‐directed alteration of the endocytic system and typify the unique intracellular locale where Salmonella replicate. A high‐throughput method devised to screen 11 520 MudJ mutants for loss of lgp‐tubule formation identified one auxotrophic and nine prototrophic mutants. Molecular characterization identified four new loci required to alter epithelial endocytic structure. Salmonella pathogenicity island 2 (SPI2) is the locus central to the phenotype. A subset of SPI2 effectors is essential: SpiC and SseFG are required, but not SseE. A subset of apparatus proteins is also implicated: SsaJ, L, M, V and P are required. SPI2 was implicated further, as SifA shows similarity with known SPI2 translocation targets, and OmpR regulates SPI2. Another locus lies within the smf–aroE intragenic region. Lgp‐tubule formation also involves a locus on the virulence plasmid pSLT. The pSLT‐encoded SpvR negatively regulates an unknown repressor of the phenotype located on pSLT. Finally, disruption of carB leads to multiple auxotrophy that prevents lgp‐tubule formation. This study demonstrates that lgp‐tubule formation is a virulence mechanism that underlies the selective disruption of host endocytic trafficking and is associated with the formation of a replication‐permissive locale.