Abstract
Roles for the non-coding small RNA RyhB in quorum-sensing and iron-dependent gene modulation in the human pathogen V. vulnificus were assessed in this study. Both the quorum sensing master regulator SmcR and the Fur-iron complex were observed to bind to the region upstream of the non-coding small RNA RyhB gene to repress expression, which suggests that RyhB is associated with both quorum-sensing and iron-dependent signaling in this pathogen. We found that expression of LuxS, which is responsible for the biosynthesis of autoinducer-2 (AI-2), was higher in wild type than in a ryhB-deletion isotype. RyhB binds directly to the 5′-UTR (untranslated region) of the luxS transcript to form a heteroduplex, which not only stabilizes luxS mRNA but also disrupts the secondary structure that normally obscures the translational start codon and thereby allows translation of LuxS to begin. The binding of RyhB to luxS mRNA requires the chaperone protein Hfq, which stabilizes RyhB. These results demonstrate that the small RNA RyhB is a key element associated with feedback control of AI-2 production, and that it inhibits quorum-sensing signaling in an iron-dependent manner. This study, taken together with previous studies, shows that iron availability and cell density signals are funneled to SmcR and RyhB, and that these regulators coordinate cognate signal pathways that result in the proper balance of protein expression in response to environmental conditions.
Highlights
Roles for the non-coding small RNA RyhB in quorum-sensing and iron-dependent gene modulation in the human pathogen V. vulnificus were assessed in this study
V. vulnificus harbors a homolog of V. harveyi luxS, which encodes an enzyme for the biosynthesis of the autoinducer-2 signaling m olecule[12,13]
Iron is not readily available in natural environments due to its low solubility at neutral p H49. It is very difficult for pathogenic bacteria to compete with host cells for iron[50]
Summary
Roles for the non-coding small RNA RyhB in quorum-sensing and iron-dependent gene modulation in the human pathogen V. vulnificus were assessed in this study. The binding of RyhB to luxS mRNA requires the chaperone protein Hfq, which stabilizes RyhB These results demonstrate that the small RNA RyhB is a key element associated with feedback control of AI-2 production, and that it inhibits quorum-sensing signaling in an iron-dependent manner. The AI-2 signal converges to LuxO, a nitrogen regulatory protein (NtrC) homolog, and is transduced to the master regulator SmcR20–22 This pathogen harbors yet another quorum-sensing pathway that is mediated by cyclic d ipeptide[23,24,25]. The sRNA chaperone Hfq is essential for this process as it binds and protects RyhB from RNase E degradation, thereby extending its half-life[34,36,37,38]
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