The
            <i>Pseudomonas aeruginosa</i>
            Magnesium Transporter MgtE Inhibits Transcription of the Type III Secretion System

Anderson, Gregory G.; Yahr, Timothy L.; Lovewell, Rustin R.; O’Toole, George A.

doi:10.1128/iai.00865-09

Cited by 38 publications

(72 citation statements)

References 52 publications

(93 reference statements)

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“…On the other hand, in P. aeruginosa, mgtE expression modulates the expression of type III secretion system (T3SS) genes, likely via inhibition of ExsA-dependent transcription. P. aeruginosa can utilize MgtE for magnesium transport and regulation of gene expression (2). Future studies in our laboratory will focus on determining the relationship between MgtE function and Serratia virulence.…”

Section: Discussionmentioning

confidence: 99%

“…For cell culture, CHO cells or the derived stably transfected CHO cells overexpressing enhanced green fluorescent protein-LC3 fusion protein (EGFP-LC3) (CHO-EGFPLC3) (64) were grown in alpha minimal essential medium (␣-MEM) supplemented with 10% (vol/vol) fetal calf serum (FCS) (both reagents obtained from Invitrogen [Argentina]) at 37°C with 5% (vol/vol) CO 2 .…”

Section: Methodsmentioning

confidence: 99%

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The PhoP/PhoQ System and Its Role in Serratia marcescens Pathogenesis

et al. 2012

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Serratia marcescens is able to invade, persist, and multiply inside nonphagocytic cells, residing in nonacidic, nondegradative, autophagosome-like vacuoles. In this work, we have examined the physiological role of the PhoP/PhoQ system and its function in the control of critical virulence phenotypes in S. marcescens . We have demonstrated the involvement of the PhoP/PhoQ system in the adaptation of this bacterium to growth on scarce environmental Mg 2+ , at acidic pH, and in the presence of polymyxin B. We have also shown that these environmental conditions constitute signals that activate the PhoP/PhoQ system. We have found that the two S. marcescens mgtE orthologs present a conserved PhoP-binding motif and demonstrated that mgtE1 expression is PhoP dependent, reinforcing the importance of PhoP control in magnesium homeostasis. Finally, we have demonstrated that phoP expression is activated intracellularly and that a phoP mutant strain is defective in survival inside epithelial cells. We have shown that the Serratia PhoP/PhoQ system is involved in prevention of the delivery to degradative/acidic compartments.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

The PhoP/PhoQ System and Its Role in Serratia marcescens Pathogenesis

et al. 2012

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“…The former includes a membrane-associated adenylcyclase (CyaB) and a cyclic AMP binding cyclic AMP receptor protein (CRP) homolog called Vfr (53), an Rhl quorum-sensing system (4,22), stationary-phase sigma factor RpoS and its transcriptional activator PsrA (22,41), and a hybrid sensor kinase/response regulator (RtsM/RetS) (19). The latter includes aceA and aceB, encoding the subunits of pyruvate dehydrogenase (11); trpA and kynA, encoding tryptophan synthase and tryptophan dioxygenase (40); truA, encoding pseudouridinase enzyme (1); and mgtE, a magnesium transporter gene (2).…”

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confidence: 99%

MexT Regulates the Type III Secretion System through MexS and PtrC in Pseudomonas aeruginosa

et al. 2011

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The type III secretion system (T3SS) is the most important virulence factor in Pseudomonas aeruginosa, and its expression level varies in different isolates. We studied the molecular basis for such differences in two laboratory strains, PAK and PAO1. A chromosomal clone library from the high-T3SS-producer strain PAK was introduced into the low-producer strain PAO1, and we found that a mexS gene from PAK confers high T3SS expression in the PAO1 background. Further tests demonstrated that both mexS and its neighboring mexT gene are required for the repression of the T3SS in PAO1, while the PAK genome encodes a defective MexS, accounting for the derepression of the T3SS in PAK and the dominant negative effect when it is introduced into PAO1. MexS is a probable oxidoreductase whose expression is dependent on MexT, a LysR-type transcriptional regulator. Various genetic data support the idea that MexS modulates the transcriptional regulator function of MexT. In searching for the MexT-dependent repressor of the T3SS, a small gene product of PA2486 (ptrC) was found effective in suppressing the T3SS upon overexpression. However, deletion of ptrC in the PAO1 background did not result in derepression of the T3SS, indicating the presence of another repressor for the T3SS. Interestingly, overexpression of functional mexS alone was sufficient to repress T3SS even in the absence of MexT, suggesting that MexS is another mediator of MexT-dependent T3SS repression. Overexpression of mexS alone had no effect on the well-known MexT-dependent genes, including those encoding MexEF efflux pump, elastase, and pyocyanin, indicating alternative regulatory mechanisms. A model has been proposed for the MexS/MexT-mediated regulation of the T3SS, the MexEF efflux pump, and the production of elastase and pyocyanin.

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“…T3SS gene expression was assessed using the P exsD-lacZ construct in WT PA14 (44). Subcultured bacteria (optical density at 600 nm [OD 600 ], ϳ0.5) were resuspended in preequilibrated HBSS buffered to the indicated pH with 25 mM HEPES, in the presence or absence of 2 mM EGTA.…”

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confidence: 99%

Acidosis Potentiates the Host Proinflammatory Interleukin-1β Response to Pseudomonas aeruginosa Infection

et al. 2014

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Infection by Pseudomonas aeruginosa, and bacteria in general, frequently promotes acidification of the local microenvironment, and this is reinforced by pulmonary exertion and exacerbation. However, the consequence of an acidic environment on the host inflammatory response to P. aeruginosa infection is poorly understood. Here we report that the pivotal cellular and host proinflammatory interleukin-1␤ (IL-1␤) response, which enables host clearance of the infection but can produce collateral inflammatory damage, is increased in response to P. aeruginosa infection within an acidic environment. Synergistic mechanisms that promote increased IL-1␤ release in response to P. aeruginosa infection in an acidic environment are increased pro-IL-1␤ induction and increased caspase-1 activity, the latter being dependent upon a functional type III secretion system of the bacteria and the NLRC4 inflammasome of the host. Using an in vivo peritonitis model, we have validated that the IL-1␤ inflammatory response is increased in mice in response to P. aeruginosa infection within an acidic microenvironment. These data reveal novel insights into the regulation and exacerbation of inflammatory responses to P. aeruginosa.

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The Pseudomonas aeruginosa Magnesium Transporter MgtE Inhibits Transcription of the Type III Secretion System

Cited by 38 publications

References 52 publications

The PhoP/PhoQ System and Its Role in Serratia marcescens Pathogenesis

The PhoP/PhoQ System and Its Role in Serratia marcescens Pathogenesis

MexT Regulates the Type III Secretion System through MexS and PtrC in Pseudomonas aeruginosa

Acidosis Potentiates the Host Proinflammatory Interleukin-1β Response to Pseudomonas aeruginosa Infection

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