Abstract
Small regulatory RNAs (sRNAs) of Shigella dysenteriae and other pathogens are vital for the regulation of virulence-associated genes and processes. Here, we characterize RyfA1, one member of a sibling pair of sRNAs produced by S. dysenteriae. Unlike its nearly identical sibling molecule, RyfA2, predicted to be encoded almost exclusively by non-pathogenic species, the presence of a gene encoding RyfA1, or a RyfA1-like molecule, is strongly correlated with virulence in a variety of enteropathogens. In S. dysenteriae, the overproduction of RyfA1 negatively impacts the virulence-associated process of cell-to-cell spread as well as the expression of ompC, a gene encoding a major outer membrane protein important for the pathogenesis of Shigella. Interestingly, the production of RyfA1 is controlled by a second sRNA, here termed RyfB1, the first incidence of one regulatory small RNA controlling another in S. dysenteriae or any Shigella species.
Highlights
Species of the bacteria Shigella (S. dysenteriae, S. sonnei, S. boydii, and S. flexneri) are the causative agents of shigellosis, a highly infectious diarrheal disease in humans
Identified by in silico-based genomic analyses designed to identify genes encoding previously uncharacterized Small regulatory RNAs (sRNAs) molecules, the putative sRNA RyfA was predicted to be encoded by Shigella flexneri and several strains of Escherichia coli [28]
Our analysis revealed that four iterations of the five‐nucleotide variable region exist in Shigella and Escherichia, three versions being grouped as “ryfA1‐like” by containing higher GC content (CACCC, CCCCC, and CGCGT) and a single ryfA2 version with higher T content (TGTTT) (Figure 4)
Summary
Species of the bacteria Shigella (S. dysenteriae, S. sonnei, S. boydii, and S. flexneri) are the causative agents of shigellosis, a highly infectious diarrheal disease in humans. Shigella infections are not limited to developing countries; the Centers for Disease Control estimates 500,000 cases of shigellosis in the United States each year [2]. Worldwide prevalence of Shigella is vast, yet universally safe treatment and prevention are lacking [1]. Of particular importance are studies that reveal the molecular mechanism underlying the ability of Shigella species to survive within the human host and cause disease. These mechanisms must be fully characterized so that they can be targeted by therapeutics, and by doing so, prevent or lessen the morbidity and mortality associated with shigellosis
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