LcrG secretion is not required for blocking of Yops secretion in Yersinia pestis

Reina, Laura D.; O'Bryant, Deanna M; Matson, Jyl S.; Nilles, Matthew L.

doi:10.1186/1471-2180-8-29

Cited by 6 publications

(12 citation statements)

References 35 publications

(58 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LcrG is cytoplasmic in all species of Yersinia , except Y. pestis , where a portion of it appears to be exported (Debord et al. , 2001; Matson and Nilles, 2001; Reina et al. , 2008).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Control of effector export by the Pseudomonas aeruginosa type III secretion proteins PcrG and PcrV

Lee

Stopford

Svenson

et al. 2010

Molecular Microbiology

View full text Add to dashboard Cite

Summary Pseudomonas aeruginosa uses a type III secretion system to inject protein effectors into a targeted host cell. Effector secretion is triggered by host cell contact. How effector secretion is prevented prior to cell contact is not well understood. In all secretion systems studied to date, the needle-tip protein is required for controlling effector secretion, but the mechanism by which needle-tip proteins control effector secretion is unclear. Here we present data that the P. aeruginosa needle-tip protein, PcrV, controls effector secretion by assembling into a functional needle-tip complex. PcrV likely does not simply obstruct the secretion channel since the pore-forming translocator proteins can still be secreted while effector secretion is repressed. This finding suggests that PcrV controls effector secretion by affecting the conformation of the apparatus, shifting it from the default, effector secretion ‘on’ conformation, to the effector secretion ‘off’ conformation. We also present evidence that PcrG, which can bind to PcrV and is also involved in controlling effector export, is cytoplasmic and that the interaction between PcrG and PcrV is not required for effector secretion control by either protein. Taken together, these data allow us to propose a working model for control of effector secretion by PcrG and PcrV.

show abstract

“…LcrG is cytoplasmic in all species of Yersinia , except Y. pestis , where a portion of it appears to be exported (Debord et al. , 2001; Matson and Nilles, 2001; Reina et al. , 2008).…”

Section: Introductionmentioning

confidence: 99%

“…, 2008). However, fusions that prevent export do not abolish its activity, suggesting that it controls effector secretion in the cytoplasm in Y. pestis as well (Reina et al. , 2008).…”

Section: Introductionmentioning

confidence: 99%

Control of effector export by the Pseudomonas aeruginosa type III secretion proteins PcrG and PcrV

Lee

Stopford

Svenson

et al. 2010

Molecular Microbiology

View full text Add to dashboard Cite

show abstract

“…(407,454). The regulatory activity of LcrG is counteracted by the tip complex protein LcrV, which interacts with LcrG in the bacterial cytoplasm (133,351,406,407).…”

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

confidence: 99%

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

359

482

View full text Add to dashboard Cite

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.

show abstract

“…The LCRS-inducing conditions cause an increase in expression of LcrV, which in turn binds to LcrG, unblocking the Ysc secretion gate. LcrG is secreted in Y. pestis, yet the secretion of LcrG is not required for blocking of the Yop secretion (Reina et al, 2008). LcrG has also been reported to bind to heparan sulphate anchored at the surface of HeLa cells, and addition of exogenous heparin and dextran sulphate strongly reduced the level of Yops' translocation into HeLa cells Sarker et al, 1998).…”

Section: Introductionmentioning

confidence: 94%

“…The hypothesis called 'titration' model has been proposed to describe the negative regulatory function of LcrG. It was suggested that LcrG acts as an 'inner gate' at the inner membrane of the bacterial cell to block the secretion channel Nilles et al, 1997;Reina et al, 2008). The LCRS-inducing conditions cause an increase in expression of LcrV, which in turn binds to LcrG, unblocking the Ysc secretion gate.…”

Section: Introductionmentioning

confidence: 99%

Gene expression profiling of Yersinia pestis with deletion of lcrG, a known negative regulator for Yop secretion of type III secretion system

Tan

Yang

et al. 2009

International Journal of Medical Microbiology

View full text Add to dashboard Cite

LcrG secretion is not required for blocking of Yops secretion in Yersinia pestis

Cited by 6 publications

References 35 publications

Control of effector export by the Pseudomonas aeruginosa type III secretion proteins PcrG and PcrV

Control of effector export by the Pseudomonas aeruginosa type III secretion proteins PcrG and PcrV

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

Gene expression profiling of Yersinia pestis with deletion of lcrG, a known negative regulator for Yop secretion of type III secretion system

Contact Info

Product

Resources

About