Regulation of Expression and Secretion of NleH, a New Non-Locus of Enterocyte Effacement-Encoded Effector in
            <i>Citrobacter rodentium</i>

García-Angulo, Víctor Antonio; Deng, Wanyin; Thomas, Nikhil A.; Finlay, B. Brett; Puente, José L.

doi:10.1128/jb.01602-07

Cited by 40 publications

(51 citation statements)

References 68 publications

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“…On the other hand, recent in vivo experiments indicated that NleHs from Citrobacter rodentium and EHEC have a role in the colonization of the gut (Garcia-Angulo et al, 2008;Hemrajani et al, 2008). In contrast with the in vitro results, NleH from C. rodentium causes an increase in NFkB activity in the colonic mucosa of NF-kB reporter mice (Hemrajani et al, 2008).…”

Section: Discussioncontrasting

confidence: 45%

Enterohaemorrhagic Escherichia coli serogroup O111 inhibits NF-κB-dependent innate responses in a manner independent of a type III secreted OspG orthologue

et al. 2009

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Enterohaemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC) inject a repertoire of effector proteins into host cells via a type III secretion system (T3SS) encoded by the locus of enterocyte effacement (LEE). OspG is an effector protein initially identified in Shigella that was shown to inhibit the host innate immune response. In this study, we found ospG homologues in EHEC (mainly of serogroup O111) and in Yersinia enterocolitica. The T3SS encoded by the LEE was able to inject these different OspG homologues into host cells. Infection of HeLa cells with EHEC O111 inhibited the NF-kB-dependent innate immune response via a T3SS-dependent mechanism. However, an EHEC O111 ospG mutant was still able to inhibit NF-kB p65 transfer to the nucleus in infected cells stimulated by tumour necrosis factor a (TNF-a). In addition, no difference in the inflammatory response was observed between wild-type EHEC O111 and the isogenic ospG mutant in the rabbit ligated intestinal loop model. These results suggest that OspG is not the sole effector protein involved in the inactivation of the host innate immune system during EHEC O111 infection.

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Section: Discussioncontrasting

confidence: 45%

Enterohaemorrhagic Escherichia coli serogroup O111 inhibits NF-κB-dependent innate responses in a manner independent of a type III secreted OspG orthologue

et al. 2009

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“…Our data indicate Tir secretion even with alteration of CesT at the C-terminal region, whereas in stark contrast, NleA secretion was impaired with CesT alteration. Other EPEC effectors have been shown to be translocated into host cells at reduced levels in the absence of CesT (64,65), indicating that CesT contributes to fully competent effector translocation. With respect to effector translocation order, the current data cannot discern the reason for the apparent preference for Tir over other effectors, although we speculate that Tir may have a high affinity for CesT that promotes its hierarchical translocation order.…”

Section: Discussionmentioning

confidence: 99%

A Novel C-Terminal Region within the Multicargo Type III Secretion Chaperone CesT Contributes to Effector Secretion

Ramu¹,

Prasad²,

Connors³

et al. 2012

Journal of Bacteriology

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The enteropathogenic Escherichia coli (EPEC) multicargo chaperone CesT interacts with at least 10 effector proteins and is central to pathogenesis. CesT has been implicated in coordinating effector hierarchy, although the mechanisms behind this regulation are poorly understood. To address this question, we set out to functionally characterize CesT with respect to roles in (i) effector binding, (ii) effector recruitment to the type III secretion system (T3SS), and (iii) effector translocation into host cells. A CesT variant expression library was screened in EPEC using a newly developed semi-high-throughput secretion assay. Among many deficient CesT variants, a predominant number were localized to a novel CesT C-terminal region. These CesT C-terminal variants exhibited normal effector binding yet reduced effector secretion levels. Structural correlation and thermal spectroscopy analyses of purified CesT variants implicated multiple surface-exposed residues, a terminal helix region, and a flexible C-terminal triple-serine stretch in effector secretion. Site-directed mutagenesis of the flexible CesT C-terminal triple-serine sequence produced differential effector secretion, implicating this region in secretion events. Infection assays further indicated that the C-terminal region of CesT was important for NleA translocation into host cells but was dispensable for Tir translocation. The findings implicate the CesT C terminus in effector secretion and contribute to a model for multiple-cargo chaperone function and effector translocation into host cells during infection.

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“…For EHEC, the regulatory circuitry controlling virulence has been intensely studied. Besides stx gene expression, the regulation of LEE-and non-LEE-encoded type III effectors is a current research topic (16,39,49).…”

Section: Discussionmentioning

confidence: 99%

“…For example, Ler and GrlA were shown to affect the expression of the non-LEE-encoded effector NleH of C. rodentium, whereas both regulators had no significant influence at the transcriptional level (16). In EHEC O157:H7, the expression and secretion of NleA were demonstrated to be regulated by Ler in a direct or indirect way (39).…”

Section: Downloaded Frommentioning

confidence: 99%

Regulation of nleA in Shiga Toxin-Producing Escherichia coli O84:H4 Strain 4795/97

2011

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Many Shiga toxin-producing Escherichia coli (STEC) strains express a type III secretion system (TTSS) encoded by the locus of enterocyte effacement (LEE). Using the TTSS, STEC is able to inject effector proteins directly into eukaryotic host cells, where they cause characteristic attaching and effacing (A/E) lesions. In addition to the LEE-encoded effectors, a number of non-LEE-encoded effectors, located on phage-associated elements, have been described. One of them, the non-LEE-encoded effector A (NleA), is widely distributed among pathogenic E. coli. In this study, we investigated the influence of environmental conditions on the expression of the phage-encoded effector nleA gene (designated nleA 4795 ) present in STEC O84:H4 strain 4795/97. We demonstrated that a particular NaCl concentration and starvation stress increase the activity of the nleA 4795 promoter. Moreover, several regulators that control nleA 4795 expression were identified. The involvement of the LEE regulators Ler, GrlA, and GrlR show that nleA 4795 is integrated in the LEE regulation circuit. Furthermore, the binding of Ler to sequences upstream of nleA 4795 underlined these findings.

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Regulation of Expression and Secretion of NleH, a New Non-Locus of Enterocyte Effacement-Encoded Effector in Citrobacter rodentium

Cited by 40 publications

References 68 publications

Enterohaemorrhagic Escherichia coli serogroup O111 inhibits NF-κB-dependent innate responses in a manner independent of a type III secreted OspG orthologue

Enterohaemorrhagic Escherichia coli serogroup O111 inhibits NF-κB-dependent innate responses in a manner independent of a type III secreted OspG orthologue

A Novel C-Terminal Region within the Multicargo Type III Secretion Chaperone CesT Contributes to Effector Secretion

Regulation of nleA in Shiga Toxin-Producing Escherichia coli O84:H4 Strain 4795/97

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