AopP, a type III effector protein of Aeromonas salmonicida, inhibits the NF-κB signalling pathway

Fehr, Désirée; Casanova, Carlo; Liverman, Amy; Blažková, Hana; Orth, Kim; Dobbelaere, Dirk; Frey, Joachim; Burr, Sarah E.

doi:10.1099/mic.0.28889-0

Cited by 86 publications

(98 citation statements)

References 39 publications

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“…HopZ1a may have originally evolved to acetylate an immunerelated kinase to suppress plant immunity similar to the function of other members of the YopJ superfamily (11,12,30,39,40). We speculate that HopZ1a-induced virulence involves manipulation of a ZED1-related kinase, in addition to other known virulence targets like microtubules (18).…”

Section: Discussionmentioning

confidence: 99%

The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a

Lewis

Lee²,

Hassan

et al. 2013

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

174

245

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Plant and animal pathogenic bacteria can suppress host immunity by injecting type III secreted effector (T3SE) proteins into host cells. However, T3SEs can also elicit host immunity if the host has evolved a means to recognize the presence or activity of specific T3SEs. The diverse YopJ/HopZ/AvrRxv T3SE superfamily, which is found in both animal and plant pathogens, provides examples of T3SEs playing this dual role. The T3SE HopZ1a is an acetyltransferase carried by the phytopathogen Pseudomonas syringae that elicits effector-triggered immunity (ETI) when recognized in Arabidopsis thaliana by the nucleotide-binding leucine-rich repeat (NB-LRR) protein ZAR1. However, recognition of HopZ1a does not require any known ETI-related genes. Using a forward genetics approach, we identify a unique ETI-associated gene that is essential for ZAR1-mediated immunity. The hopZ-ETI-deficient1 (zed1) mutant is specifically impaired in the recognition of HopZ1a, but not the recognition of other unrelated T3SEs or in pattern recognition receptor (PRR)-triggered immunity. ZED1 directly interacts with both HopZ1a and ZAR1 and is acetylated on threonines 125 and 177 by HopZ1a. ZED1 is a nonfunctional kinase that forms part of small genomic cluster of kinases in Arabidopsis. We hypothesize that ZED1 acts as a decoy to lure HopZ1a to the ZAR1-resistance complex, resulting in ETI activation.ZED1-related kinase | ZRK | hypersensitive response

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Section: Discussionmentioning

confidence: 99%

The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a

Lewis

Lee²,

Hassan

et al. 2013

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

174

245

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“…The Salmonella AvrA protein and AopP, a recently identified secreted effector from Aeromonas salmonicida (spp. Salmonicida), were also shown to inhibit activation of NF-B downstream of IKK␤ (27,43). AvrA has recently been characterized as a DUB that removes ubiquitin from I B␣ and ␤-catenin, thereby preventing their degradation and subsequent NF-B activation (13).…”

Section: Discussionmentioning

confidence: 99%

Salmonella Secreted Factor L Deubiquitinase of Salmonella typhimurium Inhibits NF-κB, Suppresses IκBα Ubiquitination and Modulates Innate Immune Responses

Negrate

Faustin

Welsh

et al. 2008

The Journal of Immunology

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134

122

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Salmonella enterica translocates virulent factors into host cells using type III secretion systems to promote host colonization, intracellular bacterial replication and survival, and disease pathogenesis. Among many effectors, the type III secretion system encoded in Salmonella pathogenicity island 2 translocates a Salmonella-specific protein, designated Salmonella secreted factor L (SseL), a putative virulence factor possessing deubiquitinase activity. In this study, we attempt to elucidate the mechanism and the function of SseL in vitro, in primary host macrophages and in vivo in infected mice. Expression of SseL in mammalian cells suppresses NF-κB activation downstream of IκBα kinases and impairs IκBα ubiquitination and degradation, but not IκBα phosphorylation. Disruption of the gene encoding SseL in S. enterica serovar typhimurium increases IκBα degradation and ubiquitination, as well as NF-κB activation in infected macrophages, compared with wild-type bacteria. Mice infected with SseL-deficient bacteria mount stronger inflammatory responses, associated with increased production of NF-κB-dependent cytokines. Thus, SseL represents one of the first bacterial deubiquitinases demonstrated to modulate the host inflammatory response in vivo.

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“…The presence of a T3SS has been reported in different A. hydrophila strains (42,46) and in the fish pathogen Aeromonas salmonicida (11). In addition, two A. hydrophila (AexT and AexU) and four A. salmonicida (AexT, AopP, AopH, and AopO) effector proteins have been identified so far (10,16,19,39,43).…”

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confidence: 99%

Aeromonas hydrophila AH-3 Type III Secretion System Expression and Regulatory Network

Vilches

Jiménez

Tomás

et al. 2009

Appl Environ Microbiol

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The Aeromonas hydrophila type III secretion system (T3SS) has been shown to play a crucial role in this pathogen's interactions with its host. We previously described the genetic organization of the T3SS cluster and the existence of at least one effector, called AexT, in A. hydrophila strain AH-3. In this study, we analyzed the expression of the T3SS regulon by analyzing the activity of the aopN-aopD and aexT promoters (T3SS machinery components and effector, respectively) by means of two different techniques: promoterless gfp fusions and real-time PCR. The expression of the A. hydrophila AH-3 T3SS regulon was induced in response to several environmental factors, of which calcium depletion, a high magnesium concentration, and a high growth temperature were shown to be the major ones. Once the optimal conditions were established, we tested the expression of the T3SS regulon in the background of several virulence determinant knockouts of strain AH-3. The analysis of the data obtained from axsA and aopN mutants, both of which have been described to be T3SS regulators in other species, allowed us to corroborate their function as the major transcription regulator and valve of the T3SS, respectively, in Aeromonas hydrophila. We also demonstrated the existence of a complicated interconnection between the expression of the T3SS and several other different virulence factors, such as the lipopolysaccharide, the PhoPQ two-component system, the ahyIR quorum sensing system, and the enzymatic complex pyruvate deshydrogenase. To our knowledge, this is the first study of the A. hydrophila T3SS regulatory network.

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AopP, a type III effector protein of Aeromonas salmonicida, inhibits the NF-κB signalling pathway

Cited by 86 publications

References 39 publications

The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a

The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a

Salmonella Secreted Factor L Deubiquitinase of Salmonella typhimurium Inhibits NF-κB, Suppresses IκBα Ubiquitination and Modulates Innate Immune Responses

Aeromonas hydrophila AH-3 Type III Secretion System Expression and Regulatory Network

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