TADB: a web-based resource for Type 2 toxin–antitoxin loci in bacteria and archaea

Shao, Yu‐Cheng; Harrison, Ewan M.; Bi, Dexi; Tai, Cui; He, Xinyi; Ou, Hong‐Yu; Rajakumar, Kumar; Deng, Zixin

doi:10.1093/nar/gkq908

Cited by 239 publications

(215 citation statements)

References 31 publications

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“…The search was based on data expanded from previous studies (99,122,136). The BLASTP program (cutoff point of 10 Ϫ4 ) was used to find homologues of the TAS families, namely, CcdAB, HicAB, HipBA, MazEF, PemIK, ParDE, Phd-Doc, RelBE, HigBA (also known as RelE-Xre [136]), YefM-YoeB, VapBC, MosAT, YeeUV, PezAT, Xre-COG2856, and Xre-Bro. Only complete TA pairs were included in this study, whereas solo toxins or solo antitoxins were excluded.…”

Section: Tas In the Genome Of S Pneumoniae: And Yet So Manymentioning

confidence: 99%

Toxin-Antitoxin Genes of the Gram-Positive Pathogen Streptococcus pneumoniae: So Few and Yet So Many

Chan

Moreno-Córdoba

Yeo

et al. 2012

Microbiol Mol Biol Rev

127

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SUMMARYPneumococcal infections cause up to 2 million deaths annually and raise a large economic burden and thus constitute an important threat to mankind. Because of the increase in the antibiotic resistance ofStreptococcus pneumoniaeclinical isolates, there is an urgent need to find new antimicrobial approaches to triumph over pneumococcal infections. Toxin-antitoxin (TA) systems (TAS), which are present in most living bacteria but not in eukaryotes, have been proposed as an effective strategy to combat bacterial infections. Type II TAS comprise a stable toxin and a labile antitoxin that form an innocuous TA complex under normal conditions. Under stress conditions, TA synthesis will be triggered, resulting in the degradation of the labile antitoxin and the release of the toxin protein, which would poison the host cells. The three functional chromosomal TAS fromS. pneumoniaethat have been studied as well as their molecular characteristics are discussed in detail in this review. Furthermore, a meticulous bioinformatics search has been performed for 48 pneumococcal genomes that are found in public databases, and more putative TAS, homologous to well-characterized ones, have been revealed. Strikingly, several unusual putative TAS, in terms of components and genetic organizations previously not envisaged, have been discovered and are further discussed. Previously, we reported a novel finding in which a unique pneumococcal DNA signature, the BOX element, affected the regulation of the pneumococcalyefM-yoeBTAS. This BOX element has also been found in some of the other pneumococcal TAS. In this review, we also discuss possible relationships between some of the pneumococcal TAS with pathogenicity, competence, biofilm formation, persistence, and an interesting phenomenon called bistability.

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Section: Tas In the Genome Of S Pneumoniae: And Yet So Manymentioning

confidence: 99%

Toxin-Antitoxin Genes of the Gram-Positive Pathogen Streptococcus pneumoniae: So Few and Yet So Many

Chan

Moreno-Córdoba

Yeo

et al. 2012

Microbiol Mol Biol Rev

127

View full text Add to dashboard Cite

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“…Although originally hypothesized to be responsible mainly for plasmid stabilization (Jensen and Gerdes 1995;Van Melderen and Saavedra De Bast 2009), these systems are now known to be involved also in anti-phage defense (Pecota and Wood 1996;Hazan and EngelbergKulka 2004;Fineran et al 2009;Koga et al 2011), antibiotics resistance via a dormant ''persistence'' behavior (Lewis 2010), and altruistic cell suicide in bacterial communities Amitai et al 2009), and are therefore attracting growing biotechnological attention . Type II toxin-antitoxin systems, in which both toxin and antitoxin are proteins, are the most widespread across bacteria, and are classified into 11 families based on protein sequence similarity (Shao et al 2011).…”

Section: New Toxin-antitoxin Systemsmentioning

confidence: 99%

A vast collection of microbial genes that are toxic to bacteria

Kimelman¹,

Levy²,

Sberro³

et al. 2012

Genome Res.

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In the process of clone-based genome sequencing, initial assemblies frequently contain cloning gaps that can be resolved using cloning-independent methods, but the reason for their occurrence is largely unknown. By analyzing 9,328,693 sequencing clones from 393 microbial genomes, we systematically mapped more than 15,000 genes residing in cloning gaps and experimentally showed that their expression products are toxic to the Escherichia coli host. A subset of these toxic sequences was further evaluated through a series of functional assays exploring the mechanisms of their toxicity. Among these genes, our assays revealed novel toxins and restriction enzymes, and new classes of small, non-coding toxic RNAs that reproducibly inhibit E. coli growth. Further analyses also revealed abundant, short, toxic DNA fragments that were predicted to suppress E. coli growth by interacting with the replication initiator DnaA. Our results show that cloning gaps, once considered the result of technical problems, actually serve as a rich source for the discovery of biotechnologically valuable functions, and suggest new modes of antimicrobial interventions.

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“…It is noteworthy that persisters occur in biofilms and planktonic cultures. Seven to twelve type II TA loci have been identified so far in the P. aeruginosa chromosome depending on the strain 11 which showed no relevance to persister formation. However, it is possible that more, as-yet-unidentified TA systems exist that are required to enter the persistent state.…”

Section: Introductionmentioning

confidence: 99%

Starvation- and antibiotics-induced formation of persister cells in Pseudomonas aeruginosa

Mlynárčik¹,

Kolář²

2017

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. Planktonic stationary and exponential cultures of Pseudomonas aeruginosa are highly resistant to killing by bactericidal antimicrobials because of the presence of persisters, cells that are multidrug tolerant and play a key role in the recalcitrance of biofilm infections. Aim. The aim of this study was to investigate the formation of persister cells in P. aeruginosa stationary vs. exponential cultures using different class antimicrobials. Methods. The susceptibilities of P. aeruginosa PAO1 wild-type and mutant strains to antimicrobials were determined by standard microtiter broth dilution method. In order to determine persister formation, dose-and time-dependent killing experiments were performed with antibiotics. Results. Ceftazidime (Cephalosporin) showed little efficacy against either culture. Stationary-phase cells were more tolerant to imipenem (Carbapenem) than exponential cells, leaving a small fraction of persisters at high imipenem concentration in both populations. Polymyxin B (Polymyxin) appeared to be ineffective at low concentrations against both cell populations. Very high polymyxin B concentration completely eradicated exponential cells and regrowth was seen in a stationary population. Stationary cells were more tolerant to tobramycin (Aminoglycoside) than exponential cells but a higher concentration of tobramycin completely eliminated survivors. Ciprofloxacin (Fluoroquinolone) at a low concentration resulted in killing of both cultures of P. aeruginosa, producing persisters that were invulnerable to killing. Conclusions. Stationary cells appear to be somewhat more tolerant than exponential cells in all of these assays. We also showed that nutrient deprivation (serine starvation) regulated by stringent and general stress response, contribute to the increased tolerance of P. aeruginosa exponential and stationary planktonic cells via production of persisters.

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TADB: a web-based resource for Type 2 toxin–antitoxin loci in bacteria and archaea

Cited by 239 publications

References 31 publications

Toxin-Antitoxin Genes of the Gram-Positive Pathogen Streptococcus pneumoniae: So Few and Yet So Many

Toxin-Antitoxin Genes of the Gram-Positive Pathogen Streptococcus pneumoniae: So Few and Yet So Many

A vast collection of microbial genes that are toxic to bacteria

Starvation- and antibiotics-induced formation of persister cells in Pseudomonas aeruginosa

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