The QseBC system was initially described as a two-component system regulated by quorum sensing, which shares homology with Salmonella enterica serovar Typhimurium PmrAB (Sperandio et al. 2002b). The same study showed that QseBC was involved in regulation of flagella and motility in EHEC.
In a detailed study (Clarke and Sperandio 2005a), it was shown that QseBC constituted a two-component system, and that the qseBC genes were cotranscribed forming an operon. Moreover, it was reported that QseB autoactivated transcription of the qseBC operon (Clarke and Sperandio 2005a). Using primer extension, the start site of the qseBC transcript was mapped, and through nested deletion analysis it was determined the minimal region necessary for QseB transcriptional auto-activation. Also, electrophoretic mobility shift assays, competition experiments, and DNAse I footprints showed that QseB directly binds to 2 sites in its own promoter.
Additionally, Clarke and Sperandio (2005b) described that QseBC regulates the flagella expression and motility through flhDC, the master regulator of flagella. Using electrophoretic mobility shift assays, competition experiments, and DNAse I footprints, it was shown that QseB directly binds to the flhDC promoter both in low and high affinity binding sites. In this study, it was also reported that the promoter of flhDC responsive to QseBC had a ct28 consensus. In summary, these studies suggested that transcription of the flhDC promoter by QseBC is a complex system and is dependent on the presence of FliA (ct28).
QseC's homologs are found at least in 25 species of bacteria, including animals and plant pathogens (Table 12.1), suggesting that this signaling system is not restricted to E. coli (Rasko et al. 2008). A few recent reports have implicated these non-EHEC qseC homologues in virulence gene activation presumably through a combination of AI-3, norepinephrine, and epinephrine activation.
Table 12.1 Some of bacterial genera and species where QseBC (Rasko et al. 2008) and QseEF two-components systems are conserved, other than EHEC
Enteropathogenic E. coli
Enteroaggregative E. coli
E. coli k12
S. enterica Typhimurium Salmonella enterica Typhi Salmonella enterica Paratyphi Shigella flexneri Shigella boydii Shigella dysenteriae Shigella sonnei Bacillus subtilis Bacillus amyloliquetaciens
The chemical structure of AI-3 was not completely elucidated yet. However, the role of epinephrine and norepinephrine has been extensively reported in different strains of E. coli, Salmonella, Staphylococcus, among others. A qseC homologue was shown to contribute to virulence in a mouse infection model of the class A bioterrorism threat agent Francisella tularensis (Weiss et al. 2007). A qseC homologue was also demonstrated to be involved in norepinephrine dependent enhancement of motility and colonization of juvenile pigs by S. enterica serovar Typhimurium (Bearson and Bearson, 2008) and virulence gene expression in this bacterium (Merighi et al. 2006; Merighi et al. 2009).
Was this article helpful?