A novel contractility pathway operating in Salmonella invasion

S. typhimurium can infect host cells not only by the well-established "trigger"-mode of invasion, inducing the formation of prominent membrane ruffles e.g., as during macropinocytosis, but also independently of these processes. Recently, we have found that the novel, ruffling-independent entry mechanism usurps the host cell contraction machinery. This mode of entry involves formation of myosin II-rich stress fiber-like structures at invasion sites, likely through stimulation of a RhoA/Rho-kinase signaling pathway and mostly downstream of the Salmonella virulence factor SopB. Importantly, this pathway operates independently of Arp2/3 complex, a central regulator of the macropinocytic entry mode. Here, we will describe our current thinking of how the contraction-dependent uptake mechanism operates to promote Salmonella invasion, and which additional cellular or bacterial factors might get engaged in the process. Finally, we will speculate on the implications of these findings for invasion by other bacterial pathogens, and discuss their impact on the canonical trigger-vs.-zipper classification of entry mechanisms employed by distinct bacterial pathogens.