Iron is both essential for and potentially toxic to bacteria, so the precise maintenance of iron homeostasis is necessary for their survival. Our previous study indicated that in the human enteropathogen Yersinia enterocolitica, the regulator OmpR directly controls the transcription of the fur, fecA and fepA genes, encoding the ferric uptake repressor and two transporters of ferric siderophores, respectively. This study was undertaken to determine the significance of the RNA chaperone Hfq and the small RNAs OmrA and RyhB1 in the post-transcriptional control of the expression of these OmpR targets. We show that Hfq silences fur, fecA and fepA expression post-transcriptionally and negatively affects the production of FLAG-tagged Fur, FecA and FepA proteins. In addition, we found that the fur gene is under the negative control of the sRNA RyhB1, while fecA and fepA are negatively regulated by the sRNA OmrA. Finally, our data revealed that the role of OmrA results from a complex interplay of transcriptional and post-transcriptional effects in the feedback circuit between the regulator OmpR and the sRNA OmrA. Thus, the expression of fur, fecA and fepA is subject to complex transcriptional and post-transcriptional regulation in order to maintain iron homeostasis in Y. enterocolitica.

Small RNAs (sRNAs) have emerged as key regulators of bacterial physiology, enabling rapid adaptation to environmental changes through post-transcriptional control. The homologous sRNAs OmrA and OmrB, conserved in Escherichia coli and other Enterobacterales, share sequence similarity yet differ in expression dynamics and functional outputs. Both act by base-pairing with target mRNAs, a process facilitated by the RNA chaperone Hfq, which promotes duplex formation and influences RNA stability. In some contexts, regulation also depends on RelA, which stabilizes Hfq-RNA complexes and links OmrA/B activity to the stringent response. Together, OmrA and OmrB modulate outer membrane protein synthesis, motility, biofilm formation, iron uptake, and virulence. OmrA is preferentially induced under nutrient limitation and integrates into the σ^S stress regulon, whereas OmrB is more broadly expressed and can engage in context-dependent mechanisms such as target sequestration. This review highlights the molecular mechanisms of OmrA/B regulation and their contribution to global sRNA-mediated regulatory networks that coordinate bacterial adaptation and pathogenicity.