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Type III secretion: a bacterial device for close combat with cells of their eukaryotic host.

ABSTRACT: Salmonella, Shigella, Yersinia, Pseudomonas aeruginosa, enteropathogenic Escherichia coli and several plant-pathogenic Gram-negative bacteria use a new type of systems called 'type III secretion' to attack their host. These systems are activated by contact with a eukaryotic cell membrane and they allow bacteria to inject bacterial proteins across the two bacterial membranes and the eukaryotic cell membrane to reach a given compartment and destroy or subvert the target cell. These systems consist of a secretion apparatus made up of about 25 individual proteins and a set of proteins released by this apparatus. Some of these released proteins are 'effectors' that are delivered by extracellular bacteria into the cytosol of the target cell while the others are 'translocators' that help the 'effectors' to cross the membrane of the eukaryotic cell. Most of the 'effectors' act on the cytoskeleton or on intracellular signalling cascades. One of the proteins injected by the enteropathogenic E. coli serves as a membrane receptor for the docking of the bacterium itself at the surface of the cell.

SUBMITTER: Cornelis GR

PROVIDER: S-EPMC1692769 | biostudies-other | 2000 May

REPOSITORIES: biostudies-other

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Type III secretion: a bacterial device for close combat with cells of their eukaryotic host.

Cornelis G R GR

Philosophical transactions of the Royal Society of London. Series B, Biological sciences 20000501 1397

Salmonella, Shigella, Yersinia, Pseudomonas aeruginosa, enteropathogenic Escherichia coli and several plant-pathogenic Gram-negative bacteria use a new type of systems called 'type III secretion' to attack their host. These systems are activated by contact with a eukaryotic cell membrane and they allow bacteria to inject bacterial proteins across the two bacterial membranes and the eukaryotic cell membrane to reach a given compartment and destroy or subvert the target cell. These systems consist ...[more]

PMID: 10874740

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Project description:Most pathogenic bacteria deliver virulence factors into host cytosol through type III secretion systems (T3SS) to perturb host immune responses. The expression of T3SS is often repressed in rich medium but is specifically induced in the host environment. The molecular mechanisms underlying host-specific induction of T3SS expression is not completely understood. Here we demonstrate in Xanthomonas citri that host-induced phosphorylation of the ATP-dependent protease Lon stabilizes HrpG, the master regulator of T3SS, conferring bacterial virulence. Ser/Thr/Tyr phosphoproteome analysis revealed that phosphorylation of Lon at serine 654 occurs in the citrus host. In rich medium, Lon represses T3SS by degradation of HrpG via recognition of its N terminus. Genetic and biochemical data indicate that phosphorylation at serine 654 deactivates Lon proteolytic activity and attenuates HrpG proteolysis. Substitution of alanine for Lon serine 654 resulted in repression of T3SS gene expression in the citrus host through robust degradation of HrpG and reduced bacterial virulence. Our work reveals a novel mechanism for distinct regulation of bacterial T3SS in different environments. Additionally, our data provide new insight into the role of protein posttranslational modification in the regulation of bacterial virulence.IMPORTANCE Type III secretion systems (T3SS) are an essential virulence trait of many bacterial pathogens because of their indispensable role in the delivery of virulence factors. However, expression of T3SS in the noninfection stage is energy consuming. Here, we established a model to explain the differential regulation of T3SS in host and nonhost environments. When Xanthomonas cells are grown in rich medium, the T3SS regulator HrpG is targeted by Lon protease for proteolysis. The degradation of HrpG leads to downregulated expression of HrpX and the hrp/hrc genes. When Xanthomonas cells infect the host, specific plant stimuli can be perceived and induce Lon phosphorylation at serine 654. Phosphorylation on Lon attenuates its proteolytic activity and protects HrpG from degradation. Consequently, enhanced stability of HrpG activates HrpX and turns on bacterial T3SS in the host. Our work provides a novel molecular mechanism underlying host-dependent activation of bacterial T3SS.

Project description:In many plant-bacterial interactions, loss of the type III secretion system (T3SS) severely reduces bacterial growth, symptom causation and suppression of defences in host plants. In the present study of Xanthomonas campestris pv. campestris (Xcc), Xcc strain B305 grew better than strain B186 in Arabidopsis thaliana after hydathode inoculation, and B305 strains mutated to the loss of T3SS (ΔhrcC and/or ΔhrpE; also ΔhrcCΔflgBC) grew similarly to wild-type B305 in Arabidopsis leaves. Unlike Xcc strain B186, wild-type B305 was relatively inefficient in secreting the exogenous T3S effector AvrBsT, but ΔhrcC and/or ΔhrpE attenuated the disease symptoms caused by Xcc B305, showing that the partially compromised T3SS of this strain still promotes necrotic leaf symptoms. In contrast with the T3SS-dependent defence suppression that has been observed for some other plant pathogenic bacteria, the Xcc B186 and B305 wild-type strains (which are virulent on Arabidopsis) caused greater elicitation of host PR-1 and PR-5 expression and callose deposition in comparison with their respective T3SS mutants. A defence-suppressing/virulence-enhancing activity of the Xcc T3SS effector suite was detectable when co-inoculation with wild-type Xcc B186 increased the growth of ΔhrcC Xcc, but this activity did not prevent the above defence elicitation. Experiments using T3SS mutants and Arabidopsis fls2 mutants suggested that FLS2 does not play a prominent role in restriction of the examined Xcc strains. However, ectopic overexpression of the Pseudomonas syringae effector AvrPto promoted in planta growth of wild-type and ΔhrcC Xcc. In summary, the T3SS components or effector suite from virulent Xcc strains elicit some host defence responses, but suppress other defences and stimulate more severe disease symptoms, AvrPto-disruptable elements other than FLS2 apparently contribute to the host restriction of Xcc, and in some virulent Xcc strains the T3SS is not absolutely required for wild-type levels of bacterial growth within the plant.

Dataset Information

Type III secretion: a bacterial device for close combat with cells of their eukaryotic host.

Publications

Type III secretion: a bacterial device for close combat with cells of their eukaryotic host.

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