FIGURE 1.

Schematic of the contribution of T3SS effectors to the intracellular lifecycle of S. Typhimurium (1). Following invasion of epithelial cells, S. Typhimurium employs the effectors SopE/E2 and SopB to transiently recruit early endosomal markers to the Salmonella-containing vacuole (SCV) (2). SCV maturation and acquisition of Rab7 lead to dynein-mediated translocation of this vacuole to the host cell perinuclear region (3). Development of the SCV into a bactericidal compartment is precluded by the action of SopB, GtgE, and SopD2, which collectively, inhibit the endosomal-lysosomal fusion activities of Rab35, Rab32, and Rab7. SseF and SseG, in complex with GCP60/ACBD3, maintain the SCV juxtanuclear position. Additionally, SifA, through its eukaryotic effector SKIP, inhibits PipB2/kinesin-1-mediated centrifugal movement of the SCV (4). Next, the SCV develops Sifs, which coincides with the onset of S. Typhimurium intravacuolar replication. Sif formation is the product of the concerted action of SifA, PipB2, and SseJ. SifA and PipB2 coordinate the centrifugal extension of the Sifs, while SifA and SseJ regulate SCV and Sif membrane dynamics that support Sif growth. Filament growth is further promoted by SptP (5). The SCV is surrounded by an actin meshwork which contributes to maintaining SCV integrity. The effectors SipA, SpvB, and SteC modulate actin dynamics in the surroundings of the SCV.