The small RNA Teg16 represses rsbV and modulates SigB-dependent gene expression in Staphylococcus aureus

Staphylococcus aureus relies on coordinated regulatory networks to adapt to environmental stress and host-associated conditions. The alternative sigma factor SigB plays a central role in this process and is controlled by the anti-anti-sigma factor RsbV, which functions as a key regulatory node in the pathway. While numerous small regulatory RNAs (sRNAs) have been identified in S. aureus , relatively few have been directly linked to the SigB stress response network. Here, we investigated the role of the small RNA Teg16 in post-transcriptional regulation of the SigB stress response pathway. Computational prediction identified a region of complementarity between Teg16 and the translational initiation region of rsbV . To test a potential regulatory effect based on this prediction, teg16 was overexpressed, and rsbV transcript levels were measured by quantitative RT-PCR. Teg16 overexpression resulted in reduced rsbV transcript levels and decreased expression of SigB-dependent genes, including asp23 and the carotenoid ( crt ) biosynthesis operon responsible for staphyloxanthin pigment production. In addition, strains carrying the teg16 expression construct exhibited altered hemolytic activity under the conditions tested, suggesting effects on virulence-associated phenotypes. We further examined whether Teg16 influences the global regulator CodY and observed reduced codY transcript levels at early time points following teg16 overexpression. Together, these results extend a previously identified regulatory relationship between Teg16 and CodY and raise the possibility of a feedback relationship linking post-transcriptional regulation to metabolic control. These findings identify Teg16 as a previously uncharacterized regulator that connects small RNA-mediated control to the SigB stress response network in S. aureus .