Abstract
The modulation of mRNA turnover is gaining recognition as a mechanism by which Staphylococcus aureus regulates gene expression, but the factors that orchestrate alterations in transcript degradation are poorly understood. In that regard, we previously found that 138 mRNA species, including transcripts coding for the virulence factors protein A (spa) and collagen-binding protein (cna), are stabilized in a sarA-dependent manner during exponential phase growth, suggesting that SarA directly or indirectly affects the RNA turnover properties of these transcripts. Herein, we expanded our characterization of the effects of sarA on mRNA turnover during late-exponential and stationary phases of growth. Results revealed that the locus affects the RNA degradation properties of cells during both growth phases. Further, using gel mobility shift assays and RIP-Chip, it was found that SarA protein is capable of binding mRNA species that it stabilizes both in vitro and within bacterial cells. Taken together, these results suggest that SarA post-transcriptionally regulates S. aureus gene expression in a manner that involves binding to and consequently altering the mRNA turnover properties of target transcripts.
Highlights
Staphylococcus aureus is a human pathogen that causes nosocomial and community-associated infections that result in high rates of morbidity and mortality (Klevens et al, 2007; Deleo et al, 2010)
It has been hypothesized that SarA regulates S. aureus gene expression via modulating the mRNA turnover properties of target transcripts
In support of this hypothesis, we have previously shown that 138 mRNA species, including the virulence factor transcripts protein A and collagen-binding protein are stabilized in a sarA-dependent manner (Roberts et al, 2006)
Summary
Staphylococcus aureus is a human pathogen that causes nosocomial and community-associated infections that result in high rates of morbidity and mortality (Klevens et al, 2007; Deleo et al, 2010). The organism largely owes its ability to cause infection to the production of an array of virulence factors which, in the laboratory setting, are coordinately regulated in a cell densitydependent manner. A plethora of two component regulatory systems (TCRS) and nucleic acid-binding proteins have been hypothesized to modulate S. aureus virulence factor expression. RNAIII has been shown to modulate virulence factor expression by directly binding to target mRNA species, thereby affecting their stability and translation properties (Morfeldt et al, 1995; Huntzinger et al, 2005; Geisinger et al, 2006; Boisset et al, 2007). RNAIII binding to the cell surface factor protein A (spa) transcript creates a substrate for ribonuclease III digestion, which, in-turn, accelerates spa mRNA digestion and limits Spa production (Huntzinger et al, 2005). Similar mechanisms of RNAIII regulation have been documented for the virulence factor coa (Chevalier et al, 2010) and the regulatory locus repressor of toxins (rot ; Boisset et al, 2007)
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