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Model for the regulatory input of H-NS in virulence, the general stress response, and motility. We propose that CRP acts through H-NS to silence virulence gene expression and enhance RpoS expression. RpoS, in turn, activates genes involved in protease production, stress response, motility, and chemotaxis. For some RpoS-dependent genes (flaA, motX, and flaC), H-NS can also act as a repressor in the absence of an active rpoS gene.
