The BarA-UvrY Two-Component System Regulates Virulence in Avian Pathogenic
            <i>Escherichia coli</i>
            O78:K80:H9

Herren, Christopher D.; Mitra, Arindam; Palaniyandi, S K; Coleman, Adam S.; Elankumaran, Subbiah; Mukhopadhyay, Suman

doi:10.1128/iai.00412-06

Cited by 64 publications

(56 citation statements)

References 62 publications

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“…Over 32 TCSs have been found in nonpathogenic E. coli that are also found in pathogenic E. coli (45). Several TCSs have been associated with the virulence of pathogenic E. coli, and a previous study demonstrated that the TCS BarA/UvrY contributes to APEC pathogenesis (24). Our microarray data showed that several target genes of TCS PhoP/PhoQ were significantly upregulated during APEC O1's growth in serum.…”

Section: Discussionmentioning

confidence: 55%

Transcriptome Analysis of Avian Pathogenic Escherichia coli O1 in Chicken Serum Reveals Adaptive Responses to Systemic Infection

Tivendale

Liu

et al. 2011

Infect Immun

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Infections of avian pathogenic Escherichia coli (APEC) result in annual multimillion-dollar losses to the poultry industry. Despite this, little is known about the mechanisms by which APEC survives and grows in the bloodstream. Thus, the aim of this study was to identify molecular mechanisms enabling APEC to survive and grow in this critical host environment. To do so, we compared the transcriptome of APEC O1 during growth in Luria-Bertani broth and chicken serum. Several categories of genes, predicted to contribute to adaptation and growth in the avian host, were identified. These included several known virulence genes and genes involved in adaptive metabolism, protein transport, biosynthesis pathways, stress resistance, and virulence regulation. Several genes with unknown function, which were localized to pathogenicity islands or APEC O1's large virulence plasmid, pAPEC-O1-ColBM, were also identified, suggesting that they too contribute to survival in serum. The significantly upregulated genes dnaK, dnaJ, phoP, and ybtA were subsequently subjected to mutational analysis to confirm their role in conferring a competitive advantage during infection. This genome-wide analysis provides novel insight into processes that are important to the pathogenesis of APEC O1.

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Section: Discussionmentioning

confidence: 55%

Transcriptome Analysis of Avian Pathogenic Escherichia coli O1 in Chicken Serum Reveals Adaptive Responses to Systemic Infection

Tivendale

Liu

et al. 2011

Infect Immun

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“…It well known that expression of bacterial virulence is regulated by conserved global systems that sense and adapt to changes in the environment. One such well-recognized system is the BarAUvrY two-component system, which has been shown to regulate APEC virulence by down-regulating type 1 and Pap fimbriae, by increasing susceptibility to oxidative stress and by reducing the amount of surface polysaccharide (Herren et al, 2006). In addition, a specific phosphate transport system (Pts) has also been linked with virulence in APEC x7122 strain (Lamarche et al, 2005).…”

Section: Progress Towards Unravelling Apec Virulence Factorsmentioning

confidence: 99%

Colibacillosis in poultry: unravelling the molecular basis of virulence of avian pathogenicEscherichia coliin their natural hosts

Dziva¹,

Stevens²

2008

Avian Pathology

303

222

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Avian colibacillosis is caused by a group of pathogens designated avian pathogenic Escherichia coli (APEC). Despite being known for over a century, avian colibacillosis remains one of the major endemic diseases afflicting the poultry industry worldwide. Autologous bacterins provide limited serotype-specific protection, yet multiple serogroups are associated with disease, especially O1, O2 and O78 among many others. Experimental infection models have facilitated the identification of some key APEC virulence genes and have allowed testing of vaccine candidates. Well-recognized virulence factors include Type 1 (F1) and P (Pap/ Prs) fimbriae for colonization, IbeA for invasion, iron acquisition systems, TraT and Iss for serum survival, K and O antigens for anti-phagocytic activity, and a temperature-sensitive haemagglutinin of imprecise function. Intriguingly, these factors do not occur universally among APEC, suggesting the presence of multiple alternative mechanisms mediating pathogenicity. The recent availability of the first complete APEC genome sequence can be expected to accelerate the identification of bacterial genes expressed during infection and required for virulence. High-throughput molecular approaches like signature-tagged transposon mutagenesis have already proved invaluable in revealing portfolios of genes expressed by pathogenic bacteria during infection, and this has enabled identification of APEC O2 factors required for septicaemia in the chicken model. Complimentary approaches, such as in vivo-induced antigen technology, exist to define the activities of APEC in vivo. In recent years, reverse vaccinology and immuno-proteomic approaches have also enabled identification of novel vaccine candidates in other bacterial pathogens. Collectively, such information provides the basis for the development or improvement of strategies to control APEC infections in the food-producing avian species.

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“…VarS/VarA homologues are found in other bacteria, including BarA/UvrY in Escherichia coli and GacS/GacA in Pseudomonas species, and these signalling systems are often involved in virulence in these other bacteria as well (Heeb & Haas, 2001;Herren et al, 2006;Pernestig et al, 2001;Tomenius et al, 2006). The signals that activate VarS/VarA-type systems have not yet been definitively established.…”

Section: Introductionmentioning

confidence: 99%

The VarS/VarA two-component system modulates the activity of the Vibrio cholerae quorum-sensing transcriptional regulator HapR

Tsou

Cai

et al. 2011

Microbiology

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The human pathogen Vibrio cholerae uses quorum sensing to regulate the expression of a number of phenotypes, including virulence factor production, in response to changes in cell density. It produces small molecules called autoinducers that increase in concentration as cell density increases, and these autoinducers bind to membrane sensors once they reach a certain threshold. This binding leads to signalling through a downstream phosphorelay pathway to alter the expression of the transcriptional regulator HapR. Previously, it was shown that the VarS/VarA two-component system acts on a component of the phosphorelay pathway upstream of HapR to regulate HapR expression levels. Here, we show that in addition to this mechanism of regulation, VarS and VarA also indirectly modulate HapR protein activity. This modulation is mediated by the small RNA CsrB but is independent of the known quorum-sensing system that links the autoinducers to HapR. Thus, the VarS/VarA two-component system intersects with the quorumsensing network at two levels. In both cases, the effect of VarS and VarA on quorum sensing is dependent on the Csr small RNAs, which regulate carbon metabolism, suggesting that V. cholerae may integrate nutrient status and cell density sensory inputs to tailor its gene expression profile more precisely to surrounding conditions.

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The BarA-UvrY Two-Component System Regulates Virulence in Avian Pathogenic Escherichia coli O78:K80:H9

Cited by 64 publications

References 62 publications

Transcriptome Analysis of Avian Pathogenic Escherichia coli O1 in Chicken Serum Reveals Adaptive Responses to Systemic Infection

Transcriptome Analysis of Avian Pathogenic Escherichia coli O1 in Chicken Serum Reveals Adaptive Responses to Systemic Infection

Colibacillosis in poultry: unravelling the molecular basis of virulence of avian pathogenicEscherichia coliin their natural hosts

The VarS/VarA two-component system modulates the activity of the Vibrio cholerae quorum-sensing transcriptional regulator HapR

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