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Summary: Bacterial pathogen Dickeya zeae strain EC1 produces antibiotics‐like phytotoxins called zeamines, which are major virulence determinants encoded by the zms gene cluster. In this study, we identified a zeamine‐deficient mutant with a Tn5 insertion in a gene designated as vfmI encoding a two‐component system (TCS) sensor histidine kinase (HK), which is accompanied by vfmH encoding a response regulator (RR) at the same genetic locus. Domain analysis shows this TCS is analogous to the VfmIH of D. dadantii, with typical characteristics of sensor HK and RR, respectively, and sharing the same operon. Deletion of either vfmI or vfmH resulted in decreased production of zeamines and cell wall degrading enzymes (CWDEs), and alleviated virulence on rice seeds and potato tubers. In D. dadantii 3937, VfmH was shown to bind to the promoters of vfmA and vfmE, while in D. zeae EC1, VfmH could bind to the promoters of vfmA, vfmE and vfmF. RNA‐seq analysis of strain EC1 and its vfmH mutant also showed that the TCS positively regulated a range of virulence genes, including zms, T1SS, T2SS, T3SS, T6SS, flagellar and CWDE genes. [ABSTRACT FROM AUTHOR]

Summary: Quorum sensing (QS) is widely utilized by bacterial pathogens to regulate biological functions and pathogenicity. Recent evidence has shown that QS is subject to regulatory cascades, especially two‐component systems that often respond to environmental stimulation. At least two different types of QS systems regulate pathogenesis in Burkholderia cenocepacia. However, it remains unclear how this bacterial pathogen controls these QS systems. Here, we demonstrate a novel two‐component system RqpSR ( Regulating Quorum sensing and Pathogenicity), which plays an important role in modulating QS and pathogenesis in B. cenocepacia. We demonstrate strong protein‐protein binding affinity between RqpS and RqpR. Mutations in rqpS and rqpR exerted overlapping effects on B. cenocepacia transcriptomes and phenotypes, including motility, biofilm formation and virulence. In trans expression of rqpR rescued the defective phenotypes in the rqpS mutant. RqpR controls target gene expression by direct binding to DNA promoters, including the cis‐2‐dodecenoic acid (BDSF) and N‐acylhomoserine lactone (AHL) signal synthase gene promoters. These findings suggest that the RqpSR system strongly modulates physiology by forming a complicated hierarchy with QS systems. This type of two‐component system appears to be widely distributed and coexists with the BDSF QS system in various bacterial species. [ABSTRACT FROM AUTHOR]

The response regulator PprB and its cognate sensor PprA were recently reported as a two-component regulatory system that controls membrane permeability and antibiotic sensitivity ofPseudomonas aeruginosa. We found that a Tn5insertion mutation inpprBcaused a drastic reduction in virulence factor production and cell motility. A transcriptome analysis revealed that 175 genes were regulated by PprB. Among the 113 PprB-activated genes, 85.5% are known to be activated byN-3-oxo-dodecanoyl-homoserine lactone (OdDHL) andN-butanoyl-homoserine lactone (BHL). In particular, the expression oflasI,rhlIandrhlR, which encode key components of thelasandrhlquorum-sensing (QS) systems, were significantly decreased in thepprBmutant. These data suggest that PprB might regulate QS signal production. Measurement of OdDHL and BHL in cultures of the mutant sustained this hypothesis. By using various OdDHL- or BHL-responsive QS reporter systems, includinglasB–lacZ,lasI–lacZandrsaL–lacZ, we found that the mutation inpprBresulted in a large decrease in the sensitivity ofP. aeruginosato exogenous OdDHL. However, there was no difference in sensitivity to BHL. Further analysis showed that the OdDHL influx was significantly reduced in thepprBmutant. We conclude that PprB is a novel QS modulator that positively regulatesN-acylhomoserine lactone production probably by affecting the OdDHL signal influx and thereby influences global expression of the QS-dependent genes. [ABSTRACT FROM AUTHOR]