Regulatory Role of PopN and Its Interacting Partners in Type III Secretion of
            <i>Pseudomonas aeruginosa</i>

Yang, Hongjing; Shan, Zhiying; Kim, Jae Wha; Wu, Weihui; Lian, Wei; Zeng, Lin; Xing, Laijun; Jin, Shouguang

doi:10.1128/jb.01680-06

Cited by 44 publications

(60 citation statements)

References 56 publications

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“…The YopN homolog PopN from P. aeruginosa blocks the secretion of effector proteins before it is itself secreted and translocated (533,611). Notably, however, in contrast to effector proteins, translocon proteins are still secreted under conditions that do not favor PopN secretion, suggesting that the negative influence of PopN on T3S is specific for effector proteins (95).…”

Section: Control Of Effector Protein Secretion In Yersinia Spp and Pmentioning

confidence: 89%

Protein Export According to Schedule: Architecture, Assembly, and Regulation of Type III Secretion Systems from Plant- and Animal-Pathogenic Bacteria

Büttner

2012

Microbiol Mol Biol Rev

366

482

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SUMMARY Flagellar and translocation-associated type III secretion (T3S) systems are present in most Gram-negative plant- and animal-pathogenic bacteria and are often essential for bacterial motility or pathogenicity. The architectures of the complex membrane-spanning secretion apparatuses of both systems are similar, but they are associated with different extracellular appendages, including the flagellar hook and filament or the needle/pilus structures of translocation-associated T3S systems. The needle/pilus is connected to a bacterial translocon that is inserted into the host plasma membrane and mediates the transkingdom transport of bacterial effector proteins into eukaryotic cells. During the last 3 to 5 years, significant progress has been made in the characterization of membrane-associated core components and extracellular structures of T3S systems. Furthermore, transcriptional and posttranscriptional regulators that control T3S gene expression and substrate specificity have been described. Given the architecture of the T3S system, it is assumed that extracellular components of the secretion apparatus are secreted prior to effector proteins, suggesting that there is a hierarchy in T3S. The aim of this review is to summarize our current knowledge of T3S system components and associated control proteins from both plant- and animal-pathogenic bacteria.

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Section: Control Of Effector Protein Secretion In Yersinia Spp and Pmentioning

confidence: 89%

Protein Export According to Schedule: Architecture, Assembly, and Regulation of Type III Secretion Systems from Plant- and Animal-Pathogenic Bacteria

Büttner

2012

Microbiol Mol Biol Rev

366

482

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“…The mexS genes from both PAO1 and PAK were cloned into the pTRG vector, and the mexT gene from PAO1 was cloned into the pBT vector. The pBT empty vector and the pTRG-mexS clone pair were used as negative controls, while the popN-TRG and pcr1-BT pair, previously shown to interact strongly (58), were used as the positive control. Test results did show a positive interaction between the MexS and MexT proteins (Fig.…”

Section: Resultsmentioning

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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“…These proteins control effector secretion from the bacterial cytoplasm (18)(19)(20). P. aeruginosa PopN and the closely related YopN associate with three other proteins that are required to prevent premature effector secretion (21)(22)(23). For PopN, these three proteins are Pcr1, Pcr2, and PscB.…”

mentioning

confidence: 99%

“…For PopN, these three proteins are Pcr1, Pcr2, and PscB. Pcr2 and PscB form a heterodimeric export chaperone, and Pcr1 is thought to tether the PopN complex to the apparatus (23). The prevailing model for explaining how PopN and related regulators control effector secretion is that they partially insert and plug the secretion channel while being tethered to the T3SS, either directly via a C-terminal interaction or indirectly via a C-terminalassociated protein, i.e., Pcr1 in P. aeruginosa (19,20).…”

mentioning

confidence: 99%

Control of type III secretion activity and substrate specificity by the cytoplasmic regulator PcrG

Lee

Zmina

Stopford

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

104

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Pathogenic Gram-negative bacteria use syringe-like type III secretion systems (T3SS) to inject effector proteins directly into targeted host cells. Effector secretion is triggered by host cell contact, and before contact is prevented by a set of conserved regulators. How these regulators interface with the T3SS apparatus to control secretion is unclear. We present evidence that the proton motive force (pmf) drives T3SS secretion in Pseudomonas aeruginosa, and that the cytoplasmic regulator PcrG interacts with distinct components of the T3SS apparatus to control two important aspects of effector secretion: (i) It coassembles with a second regulator (Pcr1) on the inner membrane T3SS component PcrD to prevent effectors from accessing the T3SS, and (ii) In conjunction with PscO, it controls protein secretion activity by modulating the ability of T3SS to convert pmf.

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Regulatory Role of PopN and Its Interacting Partners in Type III Secretion of Pseudomonas aeruginosa

Cited by 44 publications

References 56 publications

Protein Export According to Schedule: Architecture, Assembly, and Regulation of Type III Secretion Systems from Plant- and Animal-Pathogenic Bacteria

Protein Export According to Schedule: Architecture, Assembly, and Regulation of Type III Secretion Systems from Plant- and Animal-Pathogenic Bacteria

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

Control of type III secretion activity and substrate specificity by the cytoplasmic regulator PcrG

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