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The small RNA Teg41 is a pleiotropic regulator of virulence and stress response in Staphylococcus aureus

ABSTRACT: In this study, we further characterize the regulation of the αPSM transcript by Teg41. We show that a single chromosomally integrated copy of Teg41 restores virulence, hemolysis, extracellular vesicle production, and αPSM production in a strain deleted for the 3’ end of Teg41 (Teg41Δ3′ strain). We show that substituting four Teg41 nucleotides in the predicted Teg41- αPSM interaction site abolishes increased hemolysis in a Teg41 overexpression strain. We go on to demonstrte that Teg41 expression influences both the stability and abundance of the αPSM transcript, and, interestingly, that the Teg41Δ3′ strain shows decreased stability in more than 50 transcripts and altered expression levels in over 900 transcripts when compared to wild type S. aureus. Finally, we observe that Teg41 plays a role in S. aureus stress response and that the Teg41Δ3′ strain is more severely attenuated in murine systemic infection than a ∆αPSM strain, indicating that Teg41 regulation reaches beyond the αPSMs. Overall, we show that Teg41 is a unique pleiotropic sRNA in S. aureus that influences several key cellular processes.

ORGANISM(S): Staphylococcus aureus

PROVIDER: GSE185262 | GEO | 2021/10/07

REPOSITORIES: GEO

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Project description:Staphylococcus aureus is a leading cause of hospital- and community-associated infections. The organism’s ability to cause disease can, in part, be attributable to its ability to adapt to otherwise deleterious host-associated stresses. Like other bacterial species, the modulation of mRNA turnover appears to play an important role in S. aureus adaptation to certain environmental stresses. In the current study Affymetrix GeneChips® were used to examine the S. aureus responses to acid and alkaline shock-inducing conditions and to assess whether stress dependent changes in mRNA turnover are likely to facilitate the organism’s ability to tolerate extreme pH challenge. Results indicate that S. aureus adapts to pH shock by eliciting responses expected of organisms coping with pH alteration, including neutralizing cellular internal pH, DNA repair, amino acid biosynthesis and virulence factor expression. Further, it was found that the cellular response to alkaline conditions elicits a transcriptional profile that is similar to that of stringent response induced cells. Consistent with that observation, we show that the activator of the stringent response, (p)ppGpp, levels are profoundly elevated during alkaline shock conditions. We also show that the mRNA turnover properties of acid or alkaline shocked cells significantly differ from that of cells grown at neutral pH. A comparison of the mRNA degradation properties of transcripts whose titers either increased or decreased in response to sudden pH change revealed that alterations in mRNA degradation may, in part, account for the changes in the mRNA levels of factors predicted to mediate pH tolerance. Finally, a set of small stable RNA molecules were induced in response to acid or alkaline shock conditions. As in other organisms, these molecules may mediate mRNA stability and adaptation to otherwise deleterious growth conditions. Staphylococcus aureus strain UAMS-1 was grown to exponential phase and either mock treated (pH maintained at 7.4) or subjected to acid (pH 4)- or alkaline (pH 10) conditions for 30 min. Next, 200 micrograms per ml of rifampicin were added to arrest transcript synthesis. RNA was extracted from cell suspensions at 0, 2.5, 5, 15, and 30 min post-transcriptional arrest, labeled and hybridized to S. aureus GeneChips. A comparison of 0 min samples allowed assessment of acid and alkaline shock responses. A comparison of 0 min to that of various post-transcriptional arrest RNA samples allowed assessment of the mRNA turnover properties of mock vs acid or alkaline shocked cells. Duplicates of each experimental condition and corresponding post-transcriptional arrest time point were used (biological replicates).

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The small RNA Teg41 is a pleiotropic regulator of virulence and stress response in Staphylococcus aureus

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