Fig. 5. The proposed model of virulence gene regulation in Salmonella Typhimurium.

Proposed regulatory mechanism of Rof and Rho in virulence gene expression in Salmonella Typhimurium. Rho, cyan; RNAP in TEC, grey; non-template-strand DNA, template-strand DNA, and RNA, black, blue, and brick-red, respectively; PBS ligand, red; SBS ligand, green; RNA 5′ to PBS ligand, RNA between PBS ligand and SBS ligand, and spacer RNA between SBS ligand and TEC, brick-red; NusG, magenta. Upper panel (left to right). In the first step, the Rho hexamer in an open-ring state recognizes rut site (PBS ligand) through its primary binding site (PBS) on the exterior of the Rho hexamer. After a series of steps, Rho binds with short pyrimidine-rich RNA sequence (SBS ligand), changes from open-ring state to close-ring state, performs ATP-dependent 5’−3’ translocation on RNA towards the TEC, thus terminates premature transcripts and inhibits spurious transcription of SPI-1 virulence genes such as hilA, prgH, and sopB in Salmonella. Lower panel (left to right). Rof binds with Rho in its primary binding site (PBS), blocking PBS ligand RNA to bind Rho, thus prevents further transcription termination. The transcription of SPI-1 virulence genes hilA, prgH, and sopB are derepressed with reduced Rho-dependent termination.