The chromosomal <scp>SezAT</scp> toxin–antitoxin system promotes the maintenance of the <scp>SsPI</scp>‐1 pathogenicity island in epidemic <scp><i>S</i></scp><i>treptococcus suis</i>

Yao, Xinyue; Chen, Tian; Shen, Xiaodong; Zhao, Yan; Wang, Min; Rao, Xiancai; Yin, Supeng; Wang, Jing; Gong, Yanhong; Lu, Shuguang; Le, Shuai; Tan, Yinling; Tang, Jiaqi; Hu, Fuquan; Li, Ming

doi:10.1111/mmi.13116

Cited by 35 publications

(33 citation statements)

References 73 publications

(99 reference statements)

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“…Experimental evidence suggested that pezAT may play a role in stabilizing the mobile elements within the pneumococcal host (Chan et al, 2014; Iannelli et al, 2014). This suggestion coincided with a study in which a homolog of pezA T found in Streptococcus suis (termed sezAT ) was shown to be crucial for inheritance of the Pathogenicity Island (SsPI-1) during cell division (Yao et al, 2015). …”

Section: Introductionsupporting

confidence: 81%

The Streptococcus pneumoniae pezAT Toxin–Antitoxin System Reduces β-Lactam Resistance and Genetic Competence

Chan

Espinosa

2016

Front. Microbiol.

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Chromosomally encoded Type II Toxin–Antitoxin operons are ubiquitous in bacteria and archaea. Antitoxins neutralize the toxic effect of cognate Toxins by protein–protein interactions and sequestering the active residues of the Toxin. Toxins target essential bacterial processes, mostly translation and replication. However, one class apart is constituted by the PezAT pair because the PezT toxin target cell wall biosynthesis. Here, we have examined the role of the pezAT toxin–antitoxin genes in its natural host, the pathogenic bacterium Streptococcus pneumoniae. The pezAT operon on Pneumococcal Pathogenicity Island 1 was deleted from strain R6 and its phenotypic traits were compared with those of the wild type. The mutant cells formed shorter chains during exponential phase, leading to increased colony-forming units. At stationary phase, the mutant was more resilient to lysis. Importantly, the mutant exhibited higher resistance to antibiotics targeting cell walls (β-lactams), but not to antibiotics acting at other levels. In addition, the mutants also showed enhanced genetic competence. We suggest that PezAT participates in a subtle equilibrium between loss of functions (resistance to β-lactams and genetic competence) and gain of other traits (virulence).

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Section: Introductionsupporting

confidence: 81%

The Streptococcus pneumoniae pezAT Toxin–Antitoxin System Reduces β-Lactam Resistance and Genetic Competence

Chan

Espinosa

2016

Front. Microbiol.

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“…suis strain 05ZYH33 was isolated from a dead patient with STSLS during the 2005 outbreak in China and kept in our laboratory. ∆SsPI-1 was a derivative of 05ZYH33 with the entire SsPI-1 sequence replaced by a single 34 bp loxP site [16]. Whole-genome sequencing and PCR analysis confirmed that no mutations have accumulated outside the loxP site during the site-specific recombination.…”

Section: Bacterial Strains and Growth Conditionsmentioning

confidence: 93%

“…In a previous work, we demonstrated that an SsPI-1-borne toxin-antitoxin system (designated SezAT) acts as a stabilization factor assuring inheritance of SsPI-1 during cell division by killing of any descendants that are free of this element, which may drive the persistence of prevalent S. suis [16]. When devoid of a functional SezAT system, we successfully cured the entire SsPI-1 PAI from the host strain using the Cre-loxP site-specific recombination system.…”

Section: Introductionmentioning

confidence: 99%

The Impact of SsPI-1 Deletion on Streptococcus suis Virulence

Zhao

Yao

et al. 2019

Pathogens

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(1) Background: Streptococcus suis is an important zoonotic pathogen that infects pigs and can occasionally cause life-threatening systemic infections in humans. Two large-scale outbreaks of streptococcal toxic shock-like syndrome in China suggest that the pathogenicity of S. suis has been changing in recent years. Genetic analysis revealed the presence of a chromosomal pathogenicity island (PAI) designated SsPI-1 in Chinese epidemic S. suis strains. The purpose of this study is to define the role of SsPI-1 in the virulence of S. suis. (2) Methods: A SsPI-1 deletion mutant was compared to the wild-type strain regarding the ability to attach to epithelial cells, to cause host disease and mortality, and to stimulate host immune response in experimental infection of piglets. (3) Results: Deletion of SsPI-1 significantly reduces adherence of S. suis to epithelial cells and abolishes the lethality of the wild-type strain in piglets. The SsPI-1 mutant causes no significant pathological lesions and exhibits an impaired ability to induce proinflammatory cytokine production. (4) Conclusions: Deletion of the SsPI-1 PAI attenuates the virulence of this pathogen. We conclude that SsPI-1 is a critical contributor to the evolution of virulence in epidemic S. suis.

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“…The program is designed to help students understand how gene knockout occurs in bacteria through homologous recombination, using Streptococcus suis as a hands‐on instructional model. S. suis was selected because our laboratory has successfully established an efficient platform for gene targeting in this bacterium, and has published several research articles focused on its biology . The intention for developing a multiweek format was to set step‐wise learning objectives, enabling students to focus clearly on a single design objective each week, with the mastery of each subsidiary objective leading to the final desired results.…”

Section: Course Background and Learning Objectivesmentioning

confidence: 99%

Better understanding of homologous recombination through a 12‐week laboratory course for undergraduates majoring in biotechnology

Shen

Zhao

et al. 2017

Biochem Molecular Bio Educ

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Homologous recombination, a central concept in biology, is defined as the exchange of DNA strands between two similar or identical nucleotide sequences. Unfortunately, undergraduate students majoring in biotechnology often experience difficulties in understanding the molecular basis of homologous recombination. In this study, we developed and implemented a 12-week laboratory course for biotechnology undergraduates in which gene targeting in Streptococcus suis was used to facilitate their understanding of the basic concept and process of homologous recombination. Students worked in teams of two to select a gene of interest to create a knockout mutant using methods that relied on homologous recombination. By integrating abstract knowledge and practice in the process of scientific research, students gained hands-on experience in molecular biology techniques while learning about the principle and process of homologous recombination. The learning outcomes and survey-based assessment demonstrated that students substantially enhanced their understanding of how homologous recombination could be used to study gene function. Overall, the course was very effective for helping biotechnology undergraduates learn the theory and application of homologous recombination, while also yielding positive effects in developing confidence and scientific skills for future work in research. © 2017 by The International Union of Biochemistry and Molecular Biology, 45(4):329-335, 2017.

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The chromosomal SezAT toxin–antitoxin system promotes the maintenance of the SsPI‐1 pathogenicity island in epidemic Streptococcus suis

Cited by 35 publications

References 73 publications

The Streptococcus pneumoniae pezAT Toxin–Antitoxin System Reduces β-Lactam Resistance and Genetic Competence

The Streptococcus pneumoniae pezAT Toxin–Antitoxin System Reduces β-Lactam Resistance and Genetic Competence

The Impact of SsPI-1 Deletion on Streptococcus suis Virulence

Better understanding of homologous recombination through a 12‐week laboratory course for undergraduates majoring in biotechnology

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