<i>parD</i> toxin–antitoxin system of plasmid R1 – basic contributions, biotechnological applications and relationships with closely‐related toxin–antitoxin systems

Diago-Navarro, Elizabeth; Hernández‐Arriaga, Ana M.; López-Villarejo, Juan; Muñoz-Gómez, Ana J.; Kamphuis, Monique B.; Boelens, Rolf; Lemonnier, Marguerite; Dı́az-Orejas, Ramón

doi:10.1111/j.1742-4658.2010.07722.x

Cited by 32 publications

(22 citation statements)

References 142 publications

(228 reference statements)

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“…TAS were initially reported to exist on plasmids, where they function to mediate plasmid maintenance via postsegregational killing (15,16,38,60), although more subtle processes, like the coupling of plasmid replication and maintenance, have been shown for the plasmid R1-harbored kis-kid TAS (97). However, when TA genes are chromosomally carried, their function seems to be varied and debatable.…”

Section: Bacterial Tas: What Are They Really For?mentioning

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: Bacterial Tas: What Are They Really For?mentioning

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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“…Members of this Type II family share a similar fold despite low sequence similarity and different mechanisms of action. For instance, Kid and MazF toxins inhibit translation by acting as endoRNases while CcdB toxins interact with DNA gyrase and affect DNA replication [23,24,25]. Type II and Type III toxins share very low sequence similarity, e.g., only 11% identity between ToxN Pa and Kid, but their respective structures encompass a similar β core fold region surrounded by helices and loops.…”

Section: Type III Toxins Share a Common Fold And Activitymentioning

confidence: 99%

“…Type II and Type III toxins share very low sequence similarity, e.g., only 11% identity between ToxN Pa and Kid, but their respective structures encompass a similar β core fold region surrounded by helices and loops. Interestingly, despite sharing the same overall structure and the same molecular activity i.e., endoRNases, the active sites of ToxN and Kid do not match well [11,25]. Less surprisingly, differences are also found in the regions that interact with their respective antitoxins.…”

Section: Type III Toxins Share a Common Fold And Activitymentioning

confidence: 99%

Structure, Evolution, and Functions of Bacterial Type III Toxin-Antitoxin Systems

Goeders

Chai

Chen

et al. 2016

Toxins

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Toxin-antitoxin (TA) systems are small genetic modules that encode a toxin (that targets an essential cellular process) and an antitoxin that neutralises or suppresses the deleterious effect of the toxin. Based on the molecular nature of the toxin and antitoxin components, TA systems are categorised into different types. Type III TA systems, the focus of this review, are composed of a toxic endoribonuclease neutralised by a non-coding RNA antitoxin in a pseudoknotted configuration. Bioinformatic analysis shows that the Type III systems can be classified into subtypes. These TA systems were originally discovered through a phage resistance phenotype arising due to a process akin to an altruistic suicide; the phenomenon of abortive infection. Some Type III TA systems are bifunctional and can stabilise plasmids during vegetative growth and sporulation. Features particular to Type III systems are explored here, emphasising some of the characteristics of the RNA antitoxin and how these may affect the co-evolutionary relationship between toxins and cognate antitoxins in their quaternary structures. Finally, an updated analysis of the distribution and diversity of these systems are presented and discussed.

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“…Kid is a sequence-specific, translation-independent endoribonuclease whose activation inhibits the growth of plasmid-free cells [80]. The protein is a member of a broad group of structurally-related toxins that includes MazF and CcdB [1], whereas the Kis antitoxin is homologous to MazE [81].…”

Section: Phd-doc Relb-rele and Kis-kid: Transcriptional Regulatiomentioning

confidence: 99%

Regulating Toxin-Antitoxin Expression: Controlled Detonation of Intracellular Molecular Timebombs

Hayes

Kędzierska

2014

Toxins

101

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Genes for toxin-antitoxin (TA) complexes are widely disseminated in bacteria, including in pathogenic and antibiotic resistant species. The toxins are liberated from association with the cognate antitoxins by certain physiological triggers to impair vital cellular functions. TAs also are implicated in antibiotic persistence, biofilm formation, and bacteriophage resistance. Among the ever increasing number of TA modules that have been identified, the most numerous are complexes in which both toxin and antitoxin are proteins. Transcriptional autoregulation of the operons encoding these complexes is key to ensuring balanced TA production and to prevent inadvertent toxin release. Control typically is exerted by binding of the antitoxin to regulatory sequences upstream of the operons. The toxin protein commonly works as a transcriptional corepressor that remodels and stabilizes the antitoxin. However, there are notable exceptions to this paradigm. Moreover, it is becoming clear that TA complexes often form one strand in an interconnected web of stress responses suggesting that their transcriptional regulation may prove to be more intricate than currently understood. Furthermore, interference with TA gene transcriptional autoregulation holds considerable promise as a novel antibacterial strategy: artificial release of the toxin factor using designer drugs is a potential approach to induce bacterial suicide from within.

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parD toxin–antitoxin system of plasmid R1 – basic contributions, biotechnological applications and relationships with closely‐related toxin–antitoxin systems

Cited by 32 publications

References 142 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

Structure, Evolution, and Functions of Bacterial Type III Toxin-Antitoxin Systems

Regulating Toxin-Antitoxin Expression: Controlled Detonation of Intracellular Molecular Timebombs

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