Type III secretion system genes of Edwardsiella tarda associated with intracellular replication and virulence in zebrafish

Okuda, Jun; Takeuchi, Yukiko; Nakai, Toshiko

doi:10.3354/dao02763

Cited by 19 publications

(22 citation statements)

References 37 publications

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“…For some GI pathogens, in particular those for which zebrafish are not a natural host, immersion does not lead to robust intestinal colonisation (e.g., Tysnes, Jørgensen, Poppe, Midtlyng, & Robertson, 2012;Stones et al, 2017 etc.). Despite the difference in administration, these studies have contributed valuable insights into microbial factors modulating inflammation and tissue damage, which often drive mortality as a result of infection (Dong, Fan, Wang, Shi, & Zhang, 2013;Okuda, Takeuchi, & Nakai, 2014). The protozoan internalises bacteria into storage vacuoles, and following uptake of Paramecia by the zebrafish and degradation of the protozoan in the foregut, the bacterial load is released into the middle intestine.…”

Section: Adaptive Immunity and The Gi Tractmentioning

confidence: 99%

The zebrafish as a model for gastrointestinal tract–microbe interactions

Flores

Nguyen

Odem

et al. 2020

Cellular Microbiology

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The zebrafish (Danio rerio) has become a widely used vertebrate model for bacterial, fungal, viral, and protozoan infections. Due to its genetic tractability, large clutch sizes, ease of manipulation, and optical transparency during early life stages, it is a particularly useful model to address questions about the cellular microbiology of host-microbe interactions. Although its use as a model for systemic infections, as well as infections localised to the hindbrain and swimbladder having been thoroughly reviewed, studies focusing on host-microbe interactions in the zebrafish gastrointestinal tract have been neglected. Here, we summarise recent findings regarding the developmental and immune biology of the gastrointestinal tract, drawing parallels to mammalian systems. We discuss the use of adult and larval zebrafish as models for gastrointestinal infections, and more generally, for studies of host-microbe interactions in the gut. K E Y W O R D S Danio rerio, gastrointestinal tract, host-pathogen interactions, infection model, microbiome, microbiota, zebrafish

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Section: Adaptive Immunity and The Gi Tractmentioning

confidence: 99%

The zebrafish as a model for gastrointestinal tract–microbe interactions

Flores

Nguyen

Odem

et al. 2020

Cellular Microbiology

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“…The yeast strain MaV203 was transformed simultaneously with both pDBLeu-orf13 and a mouse brain cDNA fusion library inserted into the activation domain vector, pPC86 (Invitrogen). Transformants were selected using a HIS3 reporter by seeding onto selective plates containing 3AT, with MaV203 harboring both (Okuda et al 2014). (B) Western blot analysis to detect secretion of ORF13 into the culture supernatant of (left panel) the wildtype strain and (right panel) the Δorf13 mutant under TTSS-inducing conditions.…”

Section: Yeast 2-hybrid Assaymentioning

confidence: 99%

“…mET1229 is a TTSS-deficient mutant of FK1051 (Okuda et al 2006). The orf13 mutant of FK1051 (Δorf13) was a strain with an insertion mutation in the orf13 gene, and our laboratory stock strain is described by Okuda et al (2014).…”

Section: Bacterial Strains and Plasmidsmentioning

confidence: 99%

“…The E. tarda TTSS consists of 35 open reading frames (ORFs), and is essential for E. tarda survival and replication in J774 murine macrophages (Okuda et al 2006). Okuda et al (2014) reported that the 5 genes (escC, orf13, orf19, orf29, and orf30) located within the TTSS gene cluster are required both for survival and replication within J774 murine macrophages and HEp-2 human epithelial cells, and for virulence in zebrafish. In this study, we focus on the orf13 gene in the TTSS gene cluster and show that, under TTSS-inducing conditions, ORF13 was secreted into the culture supernatant and interacted with the mammalian factor Cugbp2, which regulates apoptosis in breast cancer cells.…”

Section: Introductionmentioning

confidence: 99%

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ORF13 in the Type III secretion system gene cluster of Edwardsiella tarda binds to the mammalian factor Cugbp2

Okuda

Takeuchi²,

Yasuda³

et al. 2016

Dis. Aquat. Org.

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The Type III secretion system (TTSS) is essential for the intracellular replication of Edwardsiella tarda in phagocytes of fish and mammals, and a hypothetical gene (orf13) located in the TTSS gene cluster is required for intracellular replication and virulence of E. tarda. Here, we show that under TTSS-inducing conditions, the protein ORF13 was secreted into culture supernatant. Then, using a yeast 2-hybrid screen, we show that the mammalian factor Cugbp2, which regulates apoptosis in breast cancer cells, directly interacts with ORF13. A pull-down assay revealed that ORF13 binds to the C-terminal region of Cugbp2. Our results suggest that ORF13 may facilitate E. tarda replication in phagocytes by binding to Cugbp2.KEY WORDS: Edwardsiella tarda · Type III secretion system · ORF13 · Mammalian factor Cugbp2Resale or republication not permitted without written consent of the publisher

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“…However, there are various stressful conditions such as nutrition deprivation, low pH and high reactive oxygen species (ROS) present in the intracellular niche of the phagocytes [4]. There are the strategies that virulent bacterial strains use to evade phagosomes and escape into the cytosol to enable their survival in the cells [5]. E. tarda could live and multiply in macrophages, and escape from the cells.…”

Section: Introductionmentioning

confidence: 99%

Deep Sequencing Analysis of the Eha-Regulated Transcriptome of Edwardsiella tarda Following Acidification

Gao¹,

Liu²,

Y³

et al. 2017

Metabolomics

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In response to stresses in host cells, several transcriptional regulators described in E. tarda can activate a series of interacting signaling networks [13]. Our previous study found that Eha is a transcriptional regulator of the MarR family [14]. Eha could also regulate the mRNA levels of some surface structures like the type III secretion system to affect the intracellular survival and virulence of E. tarda [15]. We found that Eha is required for the bacteria to resist oxidative stress and survive in macrophages [16]. As the type III secretion system in E. tarda disturbs the formation of the acidic environment in phagosomes [9], we hypothesized that Eha may be required for the bacteria to resist the acid stress in macrophages.Next generation sequencing technology, RNA-Sequencing (RNAseq), has been used in bacterial transcriptome analyses [17]. We performed a high-throughput RNA-seq study, which has firstly been applied in the transcriptome analyses of E. tarda, to detect and compare the differentially-expressed genes (DEGs) between the ET13 wild type bacterium and its eha mutant following exposure to acid stress. Our present study provides the gene expression profiles and sheds light on the molecular mechanism by which E. tarda survival is regulated by Eha under acid stress conditions. Key words: Eha gene; E. tarda; RNA-seq; Macrophage; Acidification IntroductionEdwardsiella tarda (E. tarda) is a facultative intracellular pathogen that causes Edwardsiellosis in freshwater and marine fish worldwide and a Salmonella-like gastroenteritis in humans [1,2]. Macrophages play critical roles in the defense against invading bacteria. Zhang et al. showed that E. tarda can utilize macrophages as a niche to initiate its virulence and spread systemic infections [3]. However, there are various stressful conditions such as nutrition deprivation, low pH and high reactive oxygen species (ROS) present in the intracellular niche of the phagocytes [4]. There are the strategies that virulent bacterial strains use to evade phagosomes and escape into the cytosol to enable their survival in the cells [5]. E. tarda could live and multiply in macrophages, and escape from the cells. It is important for the bacterium to lead to extra intestinal diseases and systemic infections [6]. E. tarda is capable to detoxify ROS by generating catalase (Kat) and superoxide dismutase (Sod) to survive within macrophages [7,8]. Okuda et al. suggested that the bacterial type III secretion system is able to interfere with the formation of acid stress in phagosomes to facilitate its replication in macrophages [9]. However, little other information is available about how E. tarda is affected by an acidic environment.Some findings have been reported about the changes that occur in other intracellular pathogens in response to acid stress in macrophages. For example, Rathman et al. suggested that an acidic environment in Salmonella-containing phagosomes is necessary for the bacterial survival and replication within the macrophage [10]. Supporting this finding, ...

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Type III secretion system genes of Edwardsiella tarda associated with intracellular replication and virulence in zebrafish

Cited by 19 publications

References 37 publications

The zebrafish as a model for gastrointestinal tract–microbe interactions

The zebrafish as a model for gastrointestinal tract–microbe interactions

ORF13 in the Type III secretion system gene cluster of Edwardsiella tarda binds to the mammalian factor Cugbp2

Deep Sequencing Analysis of the Eha-Regulated Transcriptome of Edwardsiella tarda Following Acidification

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