ArticleInfection and immunity2015
Identification and functional characterization of the novel Edwardsiella tarda effector EseJ.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 66 citations in OpenAlex.
- The Edwardsiella T3SS effector EseJ enhances NF-κB signaling by stabilizing p65 and promoting TAK1 phosphorylation.PLoS pathogens · 2026Article
- Hemolysin EthA is an Edwardsiella T3SS effector that induces PANoptosis in macrophages.Veterinary research · 2026Article
- ThemSphere · 2025Article
- T3SS effector EseJ in Edwardsiella piscicida inhibits PANoptosis in macrophages.Communications biology · 2025Article
- Presence of virulent Edwardsiella tarda in farmed nile tilapia and striped catfish.BMC microbiology · 2025Article
- The two-component system CpxAR controls biofilm formation by directly regulating the T3SS needle tip protein EseB inApplied and environmental microbiology · 2025Article
- Contrastive-learning of language embedding and biological features for cross modality encoding and effector prediction.Nature communications · 2025Article
- T3SS protein EsrC binds to theApplied and environmental microbiology · 2024Article
- Overview on the role of dietary Spirulina platensis on immune responses against Edwardsiellosis among Oreochromis niloticus fish farms.BMC veterinary research · 2024Article
- Article
- Characterization of GSDME in amphioxus provides insights into the functional evolution of GSDM-mediated pyroptosis.PLoS biology · 2023Article
- Article
- Orf1B controls secretion of T3SS proteins and contributes to Edwardsiella piscicida adhesion to epithelial cells.Veterinary research · 2022Article
- Article
- Secretion Systems in Gram-Negative Bacterial Fish Pathogens.Frontiers in microbiology · 2021Review
- Identification and Characterization of EvpQ, a Novel T6SS Effector Encoded on a Mobile Genetic Element inFrontiers in microbiology · 2021Article
- Review
- TheInfection and immunity · 2019Article
- TheApplied and environmental microbiology · 2019Article
- Edwardsiella piscicida Type III Secretion System Effector EseK Inhibits Mitogen-Activated Protein Kinase Phosphorylation and Promotes Bacterial Colonization in Zebrafish Larvae.Infection and immunity · 2018Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Edwardsiella tarda is a Gram-negative enteric pathogen that causes hemorrhagic septicemia in fish and gastro- and extraintestinal infections in humans. The type III secretion system (T3SS) of E. tarda has been identified as a key virulence factor that contributes to pathogenesis in fish. However, little is known about the associated effectors translocated by this T3SS. In this study, by comparing the profile of secreted proteins of the wild-type PPD130/91 and its T3SS ATPase ΔesaN mutant, we identified a new effector by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry. This effector consists of 1,359 amino acids, sharing high sequence similarity with Orf29/30 of E. tarda strain EIB202, and is renamed EseJ. The secretion and translocation of EseJ depend on the T3SS. A ΔeseJ mutant strain adheres to epithelioma papillosum of carp (EPC) cells 3 to 5 times more extensively than the wild-type strain does. EseJ inhibits bacterial adhesion to EPC cells from within bacterial cells. Importantly, the ΔeseJ mutant strain does not replicate efficiently in EPC cells and fails to replicate in J774A.1 macrophages. In infected J774A.1 macrophages, the ΔeseJ mutant elicits higher production of reactive oxygen species than wild-type E. tarda. The replication defect is consistent with the attenuation of the ΔeseJ mutant in the blue gourami fish model: the 50% lethal dose (LD50) of the ΔeseJ mutant is 2.34 times greater than that of the wild type, and the ΔeseJ mutant is less competitive than the wild type in mixed infection. Thus, EseJ represents a novel effector that contributes to virulence by reducing bacterial adhesion to EPC cells and facilitating intracellular bacterial replication.
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