The phosphate‐starvation response in Vibrio cholerae O1 and phoB mutant under proteomic analysis: Disclosing functions involved in adaptation, survival and virulence

Krüger, Wanda M. A. von; Lery, Letícia Miranda Santos; Soares, Márcia Regina; Neves-Manta, Fernanda; Silva, Celia Maria Batista e; Neves-Ferreira, Ana Gisele C.; Perales, Jonás; Bisch, Paulo Mascarello

doi:10.1002/pmic.200500238

Cited by 53 publications

(48 citation statements)

References 92 publications

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“…These data suggest that phoBR expression from Pho box 1 is strictly dependent on P i limitation in vivo. However, the full-length phoBR regulatory region (with boxes 1, 2, and 3; 234 bp) apparently responds to other stimuli, which could explain its small but detectable in vivo activity in P i rich medium, in agreement with previous findings (9,10,36,47,48).…”

Section: Resultssupporting

confidence: 80%

Fine-Tuning Control ofphoBRExpression in Vibrio cholerae by Binding of PhoB to Multiple Pho Boxes

Diniz

Goulart²,

Barbosa³

et al. 2011

J Bacteriol

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The control of Vibrio cholerae phoBR expression by PhoB involves its binding to Pho boxes at ؊35 (box 1), ؊60 (box 2), and ؊80 (box 3) from the putative phoB translation start site. These loci were located in the sense (box 1) and antisense (boxes 2 and 3) strands of the phoBR regulatory region, and PhoB binds to these individual boxes with distinct affinities. Fusions of sequences containing different combinations of these boxes upstream of the lacZ reporter in a plasmid demonstrated that only those carrying boxes 1, 2, and 3, or 1 alone, activated transcription under inorganic phosphate (P i ) limitation. When a fragment, including only boxes 1 and 2, was fused to lacZ, expression was no longer induced by low P i , suggesting a repressive role for PhoBϳbox2 (PhoB bound to box 2) over the transcriptional activity induced by PhoBϳbox1. The similarity between lacZ expression levels from promoter fragments containing the three boxes or box 1 alone showed that PhoBϳbox3 eliminated the repressive effect imposed by PhoBϳbox2 on phoBR transcription. Complementation assays with a phoBR-containing plasmid demonstrated that the 234-bp promoter fragment carrying the three boxes is absolutely required for operon expression in Vibrio cholerae ⌬phoBR cells. This was observed under P i abundance, when phoBR was expressed at a basal level and, also in low P i conditions, when Pho regulon genes were fully expressed. Thus, under P i limitation, PhoB exerts dual regulatory functions by binding sequentially distinct Pho boxes to enable the fine-tuning and precise control of phoBR expression in V. cholerae cells.

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Section: Resultssupporting

confidence: 80%

Fine-Tuning Control ofphoBRExpression in Vibrio cholerae by Binding of PhoB to Multiple Pho Boxes

Diniz

Goulart²,

Barbosa³

et al. 2011

J Bacteriol

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“…More recently, phosphate has also been recognized as an important nutrient and environmental signal that regulates virulence in bacteria, and a cross talk between the phosphate regulons and virulence has been suggested in various bacterial species (2,45,49,56,61).…”

Section: Resultsmentioning

confidence: 99%

RhlR Expression inPseudomonas aeruginosaIs Modulated by thePseudomonasQuinolone Signal via PhoB-Dependent and -Independent Pathways

Jensen¹,

Löns²,

Zaoui³

et al. 2006

J Bacteriol

150

147

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The expression of virulence determinants in Pseudomonas aeruginosa is coordinately regulated in response to both the social environment-commonly referred to as quorum sensing-and to environmental cues. In this study we have dissected the various independent regulation levels for pyocyanin production, which is influenced by the homoserine lactone-and Pseudomonas quinolone signal (PQS)-mediated quorum-sensing systems as well as by iron and phosphate availability. We demonstrate that the phosphate regulon is involved in the transcriptional activation of rhlR and the augmentation of PQS and pyocyanin production under phosphate limitation. However, we also observed an enhancement of rhlR transcription under low-iron medium conditions and after the addition of PQS that was independent of the phosphate regulon. These results highlight the complexity of secondary metabolite production in P. aeruginosa via environmental cues and the quorumsensing system.Bacterial organisms that elaborate traits tailored to their surroundings have better chances of surviving the pressures of unfavorable environmental conditions and host defenses. The outstanding capability of Pseudomonas aeruginosa for adaptation is reflected by the large number of putative transcriptional regulators (53), as bacterial differentiation is often controlled by transcription factors whose activity is influenced by local cues. Moreover, it has been recognized that environmental signals (33) as well as the social surrounding control bacterial virulence factor production. Cell-density-dependent gene regulation is commonly referred to as quorum sensing (QS) (20). QS is based on the release of soluble communicator molecules that trigger the transcription of QS-dependent genes when the bacterial population has reached a certain cell density. Many of these genes are involved in bacterial pathogenicity (9,19,39,40,50). Three chemically distinct signal molecules have been identified so far in P. aeruginosa. Two of these are acyl-homoserine lactones (AHL): a butyryl-homoserine lactone and a 3-oxo-dodecanoyl homoserine lactone, which together with their corresponding transcriptional activator proteins (R proteins) comprise the two hierarchically organized QS systems las and rhl (8,27,38,41,44) and control the expression of over 200 genes (23,48,57). The third signal molecule is 2-heptyl-3-hydroxy-4-quinolone (43). This Pseudomonas quinolone signal (PQS) interacts with the las and the rhl systems. While the las system seems to induce the production of PQS, exogenous PQS up-regulates the expression of the rhl system (15, 16, 31). In P. aeruginosa the impact of the rhl QS on the biosynthesis of the secondary metabolites pyocyanin and rhamnolipids is well documented (42). However, the production of these secondary metabolites also seems to be dependent on environmental cues (3,62). A link between QS and iron homeostasis was suggested previously (5,11,21,24,25,52,60). Moreover, PQS was shown to exhibit an iron-chelating activity, and PQS-dependent rhlR induction seems to be ...

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“…Loss of the Pst results in constitutive activation of the Pho regulon probably via the PhoR/PhoB two-component system, and inactivation of the regulator also influences virulence. For example, PhoB/PhoR is important for the expression of siderophores in Corynebacterium glutamicum, while hemolysin expression is PhoB dependent in Vibrio cholerae (68,69). Interestingly, defects in PhoR/B likely influence virulence through changes in cell surface components such as lipids and exopolysaccharides (59).…”

Section: Discussionmentioning

confidence: 99%

Defects in Phosphate Acquisition and Storage Influence Virulence of Cryptococcus neoformans

et al. 2014

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Nutrient acquisition and sensing are critical aspects of microbial pathogenesis. Previous transcriptional profiling indicated that the fungal pathogen Cryptococcus neoformans, which causes meningoencephalitis in immunocompromised individuals, encounters phosphate limitation during proliferation in phagocytic cells. We therefore tested the hypothesis that phosphate acquisition and polyphosphate metabolism are important for cryptococcal virulence. Deletion of the high-affinity uptake system interfered with growth on low-phosphate medium, perturbed the formation of virulence factors (capsule and melanin), reduced survival in macrophages, and attenuated virulence in a mouse model of cryptococcosis. Additionally, analysis of nutrient sensing functions for C. neoformans revealed regulatory connections between phosphate acquisition and storage and the iron regulator Cir1, cyclic AMP (cAMP)-dependent protein kinase A (PKA), and the calcium-calmodulin-activated protein phosphatase calcineurin. Deletion of the VTC4 gene encoding a polyphosphate polymerase blocked the ability of C. neoformans to produce polyphosphate. The vtc4 mutant behaved like the wild-type strain in interactions with macrophages and in the mouse infection model. However, the fungal load in the lungs was significantly increased in mice infected with vtc4 deletion mutants. In addition, the mutant was impaired in the ability to trigger blood coagulation in vitro, a trait associated with polyphosphate. Overall, this study reveals that phosphate uptake in C. neoformans is critical for virulence and that its regulation is integrated with key signaling pathways for nutrient sensing.

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The phosphate‐starvation response in Vibrio cholerae O1 and phoB mutant under proteomic analysis: Disclosing functions involved in adaptation, survival and virulence

Cited by 53 publications

References 92 publications

Fine-Tuning Control ofphoBRExpression in Vibrio cholerae by Binding of PhoB to Multiple Pho Boxes

Fine-Tuning Control ofphoBRExpression in Vibrio cholerae by Binding of PhoB to Multiple Pho Boxes

RhlR Expression inPseudomonas aeruginosaIs Modulated by thePseudomonasQuinolone Signal via PhoB-Dependent and -Independent Pathways

Defects in Phosphate Acquisition and Storage Influence Virulence of Cryptococcus neoformans

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