The different roles of hcp1 and hcp2 of the type VI secretion system in Escherichia coli strain CE129

Ding, Xueyan; Zhang, Qi; Wang, Heng; Quan, Guomei; Zhang, Dong; Ren, Wenkai; Liao, Yuexia; Xia, Pengpeng; Zhu, Guoqiang

doi:10.1002/jobm.201800156

Cited by 14 publications

(11 citation statements)

References 40 publications

(67 reference statements)

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“…In another case, the knockout of hcp1 and hcp2 genes reduced the ability of the APEC strain CE129 to infect developing chicken embryos. The expression of quorum sensing (QS)-associated genes luxS , lsrR , and pfs were downregulated in the hcp1 mutant, and the expression of type 1 fimbriae gene fimA and the adhesion-related genes fimC and papC were decreased in the hcp2 mutant, whereas the expression of antiserum survival factor genes ompA and iss were inhibited in both hcp1 and hcp2 mutants (Ding et al, 2018). Finally, fumarate and nitrate reduction (FNR), a well-known global regulator, was found to regulate expression of the T6SS, affecting the expression of vgrG in APEC (Barbieri et al, 2017).…”

Section: E Coli T6ss Acquisitionmentioning

confidence: 99%

Type VI Secretion System in Pathogenic Escherichia coli: Structure, Role in Virulence, and Acquisition

et al. 2019

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Bacterial pathogens utilize a myriad of mechanisms to invade mammalian hosts, damage tissue sites, and evade the immune system. One essential strategy of Gram-negative bacteria is the secretion of virulence factors through both inner and outer membranes to reach a potential target. Most secretion systems are harbored in mobile elements including transposons, plasmids, pathogenicity islands, and phages, and Escherichia coli is one of the more versatile bacteria adopting this genetic information by horizontal gene transfer. Additionally, E. coli is a bacterial species with members of the commensal intestinal microbiota and pathogens associated with numerous types of infections such as intestinal, urinary, and systemic in humans and other animals. T6SS cluster plasticity suggests evolutionarily divergent systems were acquired horizontally. T6SS is a secretion nanomachine that is extended through the bacterial double membrane; from this apparatus, substrates are conveyed straight from the cytoplasm of the bacterium into a target cell or to the extracellular space. This nanomachine consists of three main complexes: proteins in the inner membrane that are T4SS component-like, the baseplate complex, and the tail complex, which are formed by components evolutionarily related to contractile bacteriophage tails. Advances in the T6SS understanding include the functional and structural characterization of at least 13 subunits (so-called core components), which are thought to comprise the minimal apparatus. So far, the main role of T6SS is on bacterial competition by using it to kill neighboring non-immune bacteria for which antibacterial proteins are secreted directly into the periplasm of the bacterial target after cell–cell contact. Interestingly, a few T6SSs have been associated directly to pathogenesis, e.g., roles in biofilm formation and macrophage survival. Here, we focus on the advances on T6SS from the perspective of E. coli pathotypes with emphasis in the secretion apparatus architecture, the mechanisms of pathogenicity of effector proteins, and the events of lateral gene transfer that led to its spread.

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Section: E Coli T6ss Acquisitionmentioning

confidence: 99%

Type VI Secretion System in Pathogenic Escherichia coli: Structure, Role in Virulence, and Acquisition

et al. 2019

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“…The amino acid sequence of Hcp1 shares low identity of about 35% with the other bacteria, indicating the specificity of T6SS1; Hcp2 is highly homogenous with the protein of P. putida KT2440 K2‐T6SS (Bernal et al., 2017), suggesting the probability of similar antibacterial function; Hcp3 shares 88% identity with the corresponding protein of H2‐T6SS of P. aeruginosa (Sana et al., 2012), indicating some shared functions in virulence against eukaryotic hosts. T6SS is precisely regulated in bacteria, and Hcp expression and secretion have been recognized as the marker of a functional T6SS (Ding et al., 2018; Peng et al., 2016). In P. plecoglossicida , upregulated expression of Hcp has been observed at 18°C, suggesting that T6SSs being involved in the strong virulence at low‐temperature season (Tao et al., 2016).…”

Section: Introductionmentioning

confidence: 99%

Preliminary studies on the different roles of T6SSs in pathogenicity of Pseudomonas plecoglossicida NB2011

Jin

Huang

et al. 2021

Journal of Fish Diseases

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Pseudomonas plecoglossicida, the causative agent of visceral granulomas in the large yellow croaker (Larimichthys crocea) in China, encodes three sets of type Ⅵ secretion systems (T6SS1‐3). The purpose of this study was to characterize the different roles of T6SSs involved in infection. In‐frame deletion of T6SSs was constructed, which resulted in 8 mutants. Competition against E. coli DH5α, virulence against the croaker and in vivo survival ability of the mutants were tested. The expression and secretion of Hcp by P. plecoglossicida NB2011 were investigated. The results showed T6SS2 mutant failed to inhibit the growth of E. coli, which is an indication of T6SS2 acting against environmental bacteria. The LD50 value of T6SS1 mutant strongly increased; T6SS2 and T6SS3 mutants were similar to that of the wild type; and the virulence of double deletion or triple deletion mutant was drastically alleviated, indicating that T6SS1 being one of the major virulence factors, and T6SS2 and T6SS3 directly or indirectly being involved in the pathogenicity. T6SS1 mutant disappeared in the fish spleen in 3 days, while other strains kept increasing, indicating the T6SS1 stimulation bacteria replication in vivo. Hcp1 secreted at 12–28°C and Hcp2 secreted at 12–35°C, while Hcp3 secretion not detected in vitro. This study has thrown some insights on the understanding of pathogenicity mechanisms of this pathogen.

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“…The RNA was washed with 75% ethanol, centrifuged at 7500× g for 15 min, and dissolved in 30 μl diethyl pyrocarbonate-treated water. RNA concentration was measured using the Qubit RNA Assay Kit on a Qubit 2.0 fluorometer (Invitrogen Life Technologies), and RNA integrity was evaluated with an RNA 6000 Nano Assay Kit on a Bioanalyzer 2100 system (Agilent Technologies, Santa Clara, CA, USA) ( 41 ).…”

Section: Methodsmentioning

confidence: 99%

“…In order to validate the transcriptome sequencing results, we selected 16 DEGs for verification by qRT-PCR as previously described ( 38 , 41 ). Specific primers ( Table 1 ) were designed according to reference sequences in the NCBI database with Primer-BLAST and were synthesized by Tsingke Biotech Co (Beijing, China).…”

Section: Methodsmentioning

confidence: 99%

Transcriptomic Analysis of the Effect of GAT-2 Deficiency on Differentiation of Mice Naïve T Cells Into Th1 Cells In Vitro

et al. 2021

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The neurotransmitter γ-aminobutyric acid (GABA) is known to affect the activation and function of immune cells. This study investigated the role of GABA transporter (GAT)-2 in the differentiation of type 1 helper T (Th1) cells. Naïve CD4+ T cells isolated from splenocytes of GAT-2 knockout (KO) and wild-type (WT) mice were cultured; Th1 cell differentiation was induced and transcriptome and bioinformatics analyses were carried out. We found that GAT-2 deficiency promoted the differentiation of naïve T cells into Th1 cells. RNA sequencing revealed 2984 differentially expressed genes including 1616 that were up-regulated and 1368 that were down-regulated in GAT-2 KO cells compared to WT cells, which were associated with 950 enriched Gene Ontology terms and 33 enriched Kyoto Encyclopedia of Genes and Genomes pathways. Notably, 4 signal transduction pathways (hypoxia-inducible factor [HIF]-1, Hippo, phospholipase D, and Janus kinase [JAK]/signal transducer and activator of transcription [STAT]) and one metabolic pathway (glycolysis/gluconeogenesis) were significantly enriched by GAT-2 deficiency, suggesting that these pathways mediate the effect of GABA on T cell differentiation. Our results provide evidence for the immunomodulatory function of GABA signaling in T cell-mediated immunity and can guide future studies on the etiology and management of autoimmune diseases.

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The different roles of hcp₁ and hcp₂ of the type VI secretion system in Escherichia coli strain CE129

Cited by 14 publications

References 40 publications

Type VI Secretion System in Pathogenic Escherichia coli: Structure, Role in Virulence, and Acquisition

Type VI Secretion System in Pathogenic Escherichia coli: Structure, Role in Virulence, and Acquisition

Preliminary studies on the different roles of T6SSs in pathogenicity of Pseudomonas plecoglossicida NB2011

Transcriptomic Analysis of the Effect of GAT-2 Deficiency on Differentiation of Mice Naïve T Cells Into Th1 Cells In Vitro

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