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Novel insights into the mechanism of SepL-mediated control of effector secretion in enteropathogenic Escherichia coli.
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Knutton, S. The attaching and effacing virulence property of enteropathogenic Escherichia-coli. This Intimin-related activity was associated with Tir-dependent and -independent mechanisms thereby revealing a new property for this EPEC surface protein. Interestingly, microscopy studies identified a transient pool of Tir within the cytoplasm of epithelia infected with the Intimin-deficient, but not wildtype EPEC strain.
While Tir has been proposed to insert into the plasma membrane during the translocation process [46] , it is clear that it can insert from the host cytoplasm [47] , though an infection-associated cytoplasmic pool has, until now, only been supported by Western blot analyses [34] , [48] — [50].
It appears that Tir delivery into the host cytoplasm is normally followed by its rapid Intimin signalling-promoted association with the plasma membrane. The extended presence of Tir within the cytoplasm of eae -mutant infected cells may promote Tir-mediated loss of activation-associated TRAF2 multimers, as supported by the time course studies Fig.
Ectopically-expressed and Yersinia -delivered Tir differs from the EPEC-delivered Tir by i being mainly cytoplasmic ii only undergoing partial host kinase-mediated modification and iii failing to interact with Intimin [34] Fig. Further studies are required to define the putative EPEC factors and mechanisms involved in this regulatory process. Genome sequencing projects suggest that pathogenic E.
Thus, enterotoxigenic E. As Nle effector genes are generally missing from non-pathogenic E. The nleB1nleE1 double mutant was generated using described standard allelic exchange procedures [56] , [57] to remove confirmed by PCR analyses the entire gene sequence and inter-gene region of the adjacent nleB1 and nleE1 genes.
The nleB1nleE1tir triple mutant was generated using an available tir -deletion suicide vector as described [57]. The Yersinia strains and their usage was as previously described [34]. Caco2 parental or TC7 subclone cells were seeded at confluence onto Transwells Corning and polarised over 12—15 days as previously described [5] , [6]. Levels of firefly luciferase expression were normalised against Renilla luciferase activity as a control for transfection efficiency expressed as fold increase in luciferase activity over unstimulated control cells.
The typical optical density OD was between 0. The HeLa cell medium was replaced with DMEM at least 2 hours prior to infection routinely 3 hours unless stated otherwise , with studies on transfected cells normally 24 hours post-transfection. EPEC infections did not induce significant cell detachment under the employed experimental conditions.
When appropriate centrifugation x g 5 minutes was used to separate insoluble contains host nuclei and cytoskeleton as well as adherent bacteria and soluble contains host cytoplasmic and membrane proteins as well as T3SS-delivered proteins. Absence of reducing agents allowed the detection of TRAF2 multimeric bands. Bound antibodies were detected using horseradish peroxidase-conjugated secondary antibodies and Super Signal West Pico chemiluminescent substrate Pierce with Hyperfilm ECL Amersham Biosciences following the manufacturer's recommendations.
Supernatants 0. Following centrifugation, the unbound material was harvested and the beads washed before being resuspended in sample SDS buffer for Western blot analyses. Following experimentation, Hela cells seeded on glass coverslips were washed three times with PBS prior to fixing 2. Cells were then incubated overnight in the fridge with an appropriate primary antibody in 2.
Nuclear p65 and TRAF clusters were counted in a semi-blind fashion i. Absence of Intimin leads to a detectable pool of Tir within the host cytoplasm of infected polarised cells. Cells of the Caco-2 subclone, TC7, were seeded at confluence onto Transwells Corning for polarisation over 12—15 days.
At indicated time points, the cells were washed and processed for microscopy as described [6]. Cells infected with a tir -deficient mutant were used as the negative control to ensure background signals were zero for the wild type EPEC and eae Intimin-deficient mutant infected cells. Images show the xz-axis of the monolayer with images representative of those obtained from two independent experiments.
Tir does not induce the cellular loss of a dominant-negative variant of TRAF2. Arrow indicates a host-kinase modified Tir form, as reported [34]. We would like to acknowledge the excellent technical support provided by Sabine Quitard and contribution Fig. Wrote the paper: BK. Abstract Enteropathogenic Escherichia coli EPEC disease depends on the transfer of effector proteins into epithelia lining the human small intestine.
Introduction The EPEC disease process depends on a protein delivery system, encoded by the Locus of Enterocyte Effacement LEE Pathogenicity Island, that transfers effector proteins directly into the cytoplasm of infected epithelia [1] — [3].
Download: PPT. Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Tir interacts with TRAF2 to induce the latter's proteasomal-independent degradation. Figure 6. Figure 7. IL8 secretion assay Supernatants 0. Immuno-fluorescence microscopy Following experimentation, Hela cells seeded on glass coverslips were washed three times with PBS prior to fixing 2.
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