Abstract
Infection of the human host by Shigella species requires the coordinated production of specific Shigella virulence factors, a process mediated largely by the VirF/VirB regulatory cascade. VirF promotes the transcription of virB, a gene encoding the transcriptional activator of several virulence-associated genes. This study reveals that transcription of virB is also regulated by the small RNA RyhB, and importantly, that this regulation is not achieved indirectly via modulation of VirF activity. These data are the first to demonstrate that the regulation of virB transcription can be uncoupled from the master regulator VirF. It is also established that efficient RyhB-dependent regulation of transcription is facilitated by specific nucleic acid sequences within virB. This study not only reveals RyhB-dependent regulation of virB transcription as a novel point of control in the central regulatory circuit modulating Shigella virulence, but also highlights the versatility of RyhB in controlling bacterial gene expression.
Highlights
Shigellosis, a severe diarrheal disease caused by members of the Shigella genus (S. dysenteriae, S. flexneri, S. sonnei and S. boydii) remains a worldwide health concern with a conservative estimate of 165 million cases resulting in over one million deaths each year [1]
S. dysenteriae RyhB results in a significant decrease in the steady state level of virB mRNA, but does not influence the steady state level of virF mRNA [6]
Since all three of these possibilities are likely to lower the activity of VirF in the cell, a necessary first step in characterizing the full impact of RyhB on the VirB/VirF regulon was to determine if RyhB influences the ability of VirF to function as a transcriptional activator
Summary
Shigellosis, a severe diarrheal disease caused by members of the Shigella genus (S. dysenteriae, S. flexneri, S. sonnei and S. boydii) remains a worldwide health concern with a conservative estimate of 165 million cases resulting in over one million deaths each year [1]. Following ingestion and transit through the gastrointestinal tract of the host, Shigella invade cells of the colonic epithelium, replicate within the cytoplasm of the infected cell and spread to neighboring epithelial cells via actin based motility [2,3]. These virulenceassociated processes are mediated by the coordinated production and activity of several Shigella virulence factors. IcsA facilitates intracellular spread of Shigella by mediating actin-based motility [9], while VirB directly promotes the expression of multiple virulence-associated genes (Figure 1). As a central pathway controlling the coordinated expression of several virulenceassociated genes, any factor that influences the production or activity of VirF or VirB impacts Shigella virulence
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