Bacteriophages Carrying Shiga Toxin Genes: Genomic Variations, Detection and Potential Treatment of Pathogenic Bacteria

Łoś, Jerzy; Łoś, Marcin; Węgrzyn, Grzegorz

doi:10.2217/fmb.11.70

Cited by 61 publications

(82 citation statements)

References 128 publications

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“…According to Livny & Friedman (2004), this trait may be valuable for STEC population provided Stx production confers an advantage. The non-induced lysogens may benefit from Stx production as this toxin can cause the death of eukaryotic cells, such as unicellular predators or human leukocytes (Steinberg & Levin, 2007;Łoś et al, 2011;Mauro & Koudelka, 2011). This supports the 'model of STEC altruism' described and analysed by Łoś et al (2013).…”

Section: Induction Of Stx Phagessupporting

confidence: 72%

Shiga toxins and stx phages: highly diverse entities

2015

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Shiga toxins are the main virulence factors of a group of Escherichia coli strains [Shiga toxinproducing E. coli (STEC)] that cause severe human diseases, such as haemorrhagic colitis and haemolytic-uraemic syndrome. The Shiga toxin family comprises several toxin subtypes, which have been differentially related to clinical manifestations. In addition, the phages that carry the Shiga toxin genes (stx phages) are also diverse. These phages play an important role not only in the dissemination of Shiga toxin genes and the emergence of new STEC strains, but also in the regulation of Shiga toxin production. Consequently, differences in stx phages may affect the dissemination of stx genes as well as the virulence of STEC strains. In addition to presenting an overview of Shiga toxins and stx phages, in this review we highlight current knowledge about the diversity of stx phages, with emphasis on its impact on STEC virulence. We consider that this diversity should be taken into account when developing STEC infection treatments and diagnostic approaches, and when conducting STEC control in reservoirs.

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Section: Induction Of Stx Phagessupporting

confidence: 72%

Shiga toxins and stx phages: highly diverse entities

2015

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“…Shiga toxin-converting bacteriophages (or Stx phages) are classified as lambdoid viruses due to organization of their genomes, which resembles that of bacteriophage l (Allison, 2007;Łoś et al, 2011). Although there are also homologies between sequences of some crucial regulatory genes of Stx phages and l, they rarely share a common virion structure.…”

Section: Introductionmentioning

confidence: 99%

“…Although there are also homologies between sequences of some crucial regulatory genes of Stx phages and l, they rarely share a common virion structure. Nevertheless, similarities in regulatory mechanisms of viral development are also evident, including the lysis-versuslysogenization decision, control of phage gene expression and phage DNA replication; though differences in important details were also reported (Ptashne, 2004;Węgrzyn & Węgrzyn, 2005;Węgrzyn et al, 2012;Allison, 2007;Nejman et al, 2009;Łoś et al, 2011;Riley et al, 2012). What clearly distinguishes all Stx phages from l is the presence of stx genes, coding for Shiga toxins, in their genomes.…”

Section: Introductionmentioning

confidence: 99%

Defects in RNA polyadenylation impair both lysogenization by and lytic development of Shiga toxin-converting bacteriophages

Nowicki

Bloch

Nejman-Faleńczyk

et al. 2015

Journal of General Virology

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In Escherichia coli, the major poly(A) polymerase (PAP I) is encoded by the pcnB gene. In this report, a significant impairment of lysogenization by Shiga toxin-converting (Stx) bacteriophages (W24 B , 933W, P22, P27 and P32) is demonstrated in host cells with a mutant pcnB gene. Moreover, lytic development of these phages after both infection and prophage induction was significantly less efficient in the pcnB mutant than in the WT host. The increase in DNA accumulation of the Stx phages was lower under conditions of defective RNA polyadenylation. Although shortly after prophage induction, the levels of mRNAs of most phage-borne early genes were higher in the pcnB mutant, at subsequent phases of the lytic development, a drastically decreased abundance of certain mRNAs, including those derived from the N, O and Q genes, was observed in PAP I-deficient cells. All of these effects observed in the pcnB cells were significantly more strongly pronounced in the Stx phages than in bacteriophage l. Abundance of mRNA derived from the pcnB gene was drastically increased shortly (20 min) after prophage induction by mitomycin C and decreased after the next 20 min, while no such changes were observed in non-lysogenic cells treated with this antibiotic. This prophage induction-dependent transient increase in pcnB transcript may explain the polyadenylation-driven regulation of phage gene expression.

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“…These genes are inserted into genomes of lambdoid bacteriophages (viruses related to members of the family) that can lysogenize E. coli strains and are called Shiga toxin-converting bacteriophages (5,6). In all STEC strains analyzed to date, the stx genes are under the control of the late phage promoter, called p R = (7,8).…”

mentioning

confidence: 99%

“…Thus, in bacteria lysogenic for Shiga toxin-converting bacteriophages, expression of the stx genes is blocked, and production of Shiga toxins must be preceded by prophage induction (11,12). Moreover, after prophage induction, effective expression of stx genes by the host cell depends on efficient phage DNA replication and resultant multiple copies of these genes (6).…”

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confidence: 99%

ppGpp-Dependent Negative Control of DNA Replication of Shiga Toxin-Converting Bacteriophages in Escherichia coli

et al. 2013

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bThe pathogenicity of enterohemorrhagic Escherichia coli (EHEC) strains depends on the production of Shiga toxins that are encoded on lambdoid prophages. Effective production of these toxins requires prophage induction and subsequent phage replication. Previous reports indicated that lytic development of Shiga toxin-converting bacteriophages is inhibited in amino acidstarved bacteria. However, those studies demonstrated that inhibition of both phage-derived plasmid replication and production of progeny virions occurred during the stringent as well as the relaxed response to amino acid starvation, i.e., in the presence as well as the absence of high levels of ppGpp, an alarmone of the stringent response. Therefore, we asked whether ppGpp influences DNA replication and lytic development of Shiga toxin-converting bacteriophages. Lytic development of 5 such bacteriophages was tested in an E. coli wild-type strain and an isogenic mutant that does not produce ppGpp (ppGpp 0 ). In the absence of ppGpp, production of progeny phages was significantly (in the range of an order of magnitude) more efficient than in wild-type cells. Such effects were observed in infected bacteria as well as after prophage induction. All tested bacteriophages formed considerably larger plaques on lawns formed by ppGpp 0 bacteria than on those formed by wild-type E. coli. The efficiency of synthesis of phage DNA and relative amount of lambdoid plasmid DNA were increased in cells devoid of ppGpp relative to bacteria containing a basal level of this nucleotide. We conclude that ppGpp negatively influences the lytic development of Shiga toxin-converting bacteriophages and that phage DNA replication efficiency is limited by the stringent control alarmone.

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Bacteriophages Carrying Shiga Toxin Genes: Genomic Variations, Detection and Potential Treatment of Pathogenic Bacteria

Cited by 61 publications

References 128 publications

Shiga toxins and stx phages: highly diverse entities

Shiga toxins and stx phages: highly diverse entities

Defects in RNA polyadenylation impair both lysogenization by and lytic development of Shiga toxin-converting bacteriophages

ppGpp-Dependent Negative Control of DNA Replication of Shiga Toxin-Converting Bacteriophages in Escherichia coli

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