VopB1 and VopD1 are essential for translocation of type III secretion system 1 effectors of <i>Vibrio parahaemolyticus</i>

Shimohata, Takaaki; Mawatari, Kazuaki; Iba, Hitomi; Hamano, Masakazu; Negoro, Sachie; Asada, Shoko; Aihara, Mutsumi; Hirata, Akiko; Su, Zehong; Takahashi, Akira

doi:10.1139/w2012-081

Cited by 10 publications

(5 citation statements)

References 24 publications

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“…However, it remains to be determined whether EseE controls the transcription of the escC-eseE operon through interaction with an unknown transcriptional factor. T3SS translocon proteins are essential for effector translocation but are dispensable for effector secretion (10,38). Similarly, the deletion of eseB abolishes the translocation of EseJ in E. tarda (10).…”

Section: Discussionmentioning

confidence: 99%

EseE of Edwardsiella tarda Augments Secretion of Translocon Protein EseC and Expression of the escC - eseE Operon

et al. 2016

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Edwardsiella tarda is an important Gram-negative pathogen that employs a type III secretion system (T3SS) to deliver effectors into host cells to facilitate bacterial survival and replication. These effectors are translocated into host cells through a translocon complex composed of three secreted proteins, namely, EseB, EseC, and EseD. The secretion of EseB and EseD requires a chaperone protein called EscC, whereas the secretion of EseC requires the chaperone EscA. In this study, we identified a novel protein (EseE) that also regulates the secretion of EseC. An eseE deletion mutant secreted much less EseC into supernatants, accompanied by increased EseC levels within bacterial cells. We also demonstrated that EseE interacted directly with EseC in a pulldown assay. Interestingly, EseC, EseE, and EscA were able to form a ternary complex, as revealed by pulldown and gel filtration assays. Of particular importance, the deletion of eseE resulted in decreased levels of EseB and EseD proteins in both the bacterial pellet and supernatant fraction. Furthermore, real-time PCR assays showed that EseE positively regulated the transcription of the translocon operon escC-eseE, comprising escC, eseB, escA, eseC, eseD, and eseE. These effects of EseE on the translocon components/operon appeared to have a functional consequence, since the ⌬eseE strain was outcompeted by wild-type E. tarda in a mixed infection in blue gourami fish. Collectively, our results demonstrate that EseE not only functions as a chaperone for EseC but also acts as a positive regulator controlling the expression of the translocon operon escC-eseE, thus contributing to the pathogenesis of E. tarda in fish.T he type III secretion system (T3SS) is a contact-dependent translocation system. It forms a syringe-like structure spanning the inner and outer membranes of bacteria and induces pore formation on host cells (1). Through these pores, an array of bacterial proteins (effectors) are delivered into host cells, where they manipulate host cell signaling pathways to promote bacterial survival (2).Edwardsiella tarda is a Gram-negative intracellular pathogen that can cause hemorrhagic septicemia in fish (3), as well as gastroand extraintestinal infections in humans (4, 5). The T3SS is well known to be one of the most important virulence factors in E. tarda (6, 7). It facilitates the survival and replication of E. tarda in host cells (6-9). E. tarda T3SS contains 34 open reading frames (ORFs), which encode the apparatus, chaperones, effectors, and regulators (6, 10). The expression of E. tarda T3SS is controlled by many factors, such as the two-component system esrA-esrB (6) and esrC (11) inside the T3SS gene cluster, as well as phoP-phoQ (12) and phoR-phoB (13) located outside the T3SS gene cluster. Intriguingly, our group recently showed that a type III secretion system-secreted protein (EscE) also functions as a regulator controlling the injection of effectors and secretion of translocators (14).EseB, EseC, and EseD, secreted by the E. tarda T3SS, are homologous ...

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Section: Discussionmentioning

confidence: 99%

EseE of Edwardsiella tarda Augments Secretion of Translocon Protein EseC and Expression of the escC - eseE Operon

et al. 2016

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“…T3SS1 is mainly responsible for V. parahaemolyticus cytotoxicity. To better understand how the LuxQ-ArcB-LuxO pathway regulates the cytotoxicity of V. parahaemolyticus under aerobic conditions, we selected several T3SS1 genes for transcriptional analysis, including those that encode the translocon proteins VopB1 and VopD1, 64 the T3SS1 regulators ExsA and ExsD, 11 the effector proteins VopS and VopQ, 65 and the structural proteins VscC1 and VcrD1. 55 Transcription levels for these genes were significantly downregulated in the deletion strains (Δ luxQ , Δ luxO , Δ arcB , Δ arcB Δ luxQ , Δ luxQ Δ luxO , and Δ arcB Δ luxO ) compared to those in the WT strain and the complemented strains (Δ luxQ :BBR- luxQ , Δ luxO :BBR- luxO , and Δ arcB :BBR- arcB ) ( Figure 7 and S6).…”

Section: Resultsmentioning

confidence: 99%

ArcB orchestrates the quorum-sensing system to regulate type III secretion system 1 in Vibrio parahaemolyticus

Zhang,

Liu,

et al. 2023

Gut Microbes

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In many Vibrio species, virulence is regulated by quorum sensing, which is regulated by a complex, multichannel, two-component phosphorelay circuit. Through this circuit, sensor kinases transmit sensory information to the phosphotransferase LuxU via a phosphotransfer mechanism, which in turn transmits the signal to the response regulator LuxO. For Vibrio parahaemolyticus , type III secretion system 1 (T3SS1) is required for cytotoxicity, but it is unclear how quorum sensing regulates T3SS1 expression. Herein, we report that a hybrid histidine kinase, ArcB, instead of LuxU, and sensor kinase LuxQ and response regulator LuxO, collectively orchestrate T3SS1 expression in V. parahaemolyticus . Under high oxygen conditions, LuxQ can interact with ArcB directly and phosphorylates the Hpt domain of ArcB. The Hpt domain of ArcB phosphorylates the downstream response regulator LuxO instead of ArcA. LuxO then activates transcription of the T3SS1 gene cluster. Under hypoxic conditions, ArcB autophosphorylates and phosphorylates ArcA, whereas ArcA does not participate in regulating the expression of T3SS1. Our data provides evidence of an alternative regulatory path involving the quorum sensing phosphorelay and adds another layer of understanding about the environmental regulation of gene expression in V. parahaemolyticus .

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“…However, after cold shock, T3SS genes ( vcrD1 , vcrD2β and vopD1 ) were down-regulated. Earlier studies showed that vcrD1 and vcrD2β encodes for an inner membrane protein [41], and vopD1 is essential for translocation of T3SS1 effector of V. parahaemolyticus [42]. Compared with 4 °C and 10 °C, the genes expression of flagella (pilA), QS (aphA, opaR) and virulence (trh) at 37 °C are significantly higher.…”

Section: Resultsmentioning

confidence: 99%

Cold Shock Fail to Restrain Pre-formedVibrio parahaemolyticusBiofilm

Qiao

Song

et al. 2019

Preprint

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19The source of persistent infections can be biofilms that occur naturally on food surfaces and 20 medical biomaterials. Biofilm formation on these materials are likely to be affected by 21 environmental temperature fluctuations and information on noticeable temperature shifts on 22 the fate of pre-formed biofilm is sparse. Changes to pre-formed Vibrio parahaemolyticus 23 biofilm under cold shock (4 °C and 10 °C) was explored in this study. We show that V. 24 parahaemolyticus biofilm biomass increased significantly during this cold shock period and 25 there was a gradual increase of polysaccharides and proteins content in the extracellular 26 polymeric matrix (EPS). In addition, we demonstrate that the expression of flagella and 27 virulence-related genes were differentially regulated. The architecture of the biofilm, 28 quantified using mean thickness (MT), average diffusion distance (ADD), porosity (P), 29 biofilm roughness (BR) and homogeneity (H) also changed during the cold shock and these 30 parameters were correlated (P < 0.01). However, the correlation between biofilm architecture 31 and biofilm-related genes expression was relatively weak (P < 0.05). Cold shock at 4 °C and 32 10 °C is not sufficient to reduce V. parahaemolyticus biofilm formation and strategies to 33 reduce risk of foodborne infections should take this information into account. 34 35

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VopB1 and VopD1 are essential for translocation of type III secretion system 1 effectors of Vibrio parahaemolyticus

Cited by 10 publications

References 24 publications

EseE of Edwardsiella tarda Augments Secretion of Translocon Protein EseC and Expression of the escC - eseE Operon

EseE of Edwardsiella tarda Augments Secretion of Translocon Protein EseC and Expression of the escC - eseE Operon

ArcB orchestrates the quorum-sensing system to regulate type III secretion system 1 in Vibrio parahaemolyticus

Cold Shock Fail to Restrain Pre-formedVibrio parahaemolyticusBiofilm

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