Molecular Insights Into the Evolutionary Pathway of Vibrio cholerae O1 Atypical El Tor Variants

Kim, Eun Jin; Lee, Dokyung; Moon, Se Hoon; Lee, Chan Hee; Kim, Sang Jun; Lee, Jae Hyun; Kim, Jae Ouk; Song, Manki; Das, Bhabatosh; Clemens, John D.; Pape, Jean William; Nair, G. Balakrish; Kim, Dong Wook

doi:10.1371/journal.ppat.1004384

Cited by 40 publications

(65 citation statements)

References 32 publications

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“…The replication and dissemination of CTX-2 phage have been demonstrated under laboratory conditions in this report (3,16). Because of the absence of classical biotype strains that contain a tandem repeat of lysogenic CTX-cla, the replication of lysogenic CTX-cla has not been provided in this report; however, the presence of a tandem repeat of CTX-2 in Wave 2 atypical El Tor strains suggests that classical strains that harbor a tandem repeat of CTX-cla existed.…”

Section: Discussionmentioning

confidence: 79%

“…S1). A zot-3′UTR fragment that spans nucleotide 245 of zot to the termination codon of rstR El Tor of RS1 was amplified by PCR with the primer pair zot-MluIF (CGC GCG ACG CGT TTC TCT TTA TCG ATG) and 3′UTR-KpnIR (CCG GCC GGT ACC CAA GAC TCG CTA GCG) from the strain PM8, which contains TLC:CTX-1kan:RS1 on chromosome 1 (16). This fragment was common to all CTX phages that were constructed in this study.…”

Section: Methodsmentioning

confidence: 99%

“…Replication of CTX-2 from a tandem repeat of lysogenic CTX-2 on chromosome 2 in Wave 2 El Tor strains was also substantiated. PM9 and PM22, derivatives of V212-1 and B33, respectively, were constructed as described previously (16). Approximately 10 3 transductants were obtained from the primary transduction of PM9 and PM22 (Table 1 and 2).…”

Section: Ctx-2 Replication From the Tandem Repeat Of Lysogenic Ctx-2 Inmentioning

confidence: 99%

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Replication of Vibrio cholerae classical CTX phage

Kim

Lee

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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The toxigenic classical and El Tor biotype Vibrio cholerae serogroup O1 strains are generated by lysogenization of host-type-specific cholera toxin phages (CTX phages). Experimental evidence of the replication and transmission of an El Tor biotype-specific CTX phage, CTX-1, has explained the evolution of V. cholerae El Tor biotype strains. The generation of classical biotype strains has not been demonstrated in the laboratory, and the classical biotypespecific CTX phage, CTX-cla, is considered to be defective with regard to replication. However, the identification of atypical El Tor strains that contain CTX-cla-like phage, CTX-2, indicates that CTX-cla and CTX-2 replicate and can be transmitted to V. cholerae strains. The replication of CTX-cla and CTX-2 phages and the transduction of El Tor biotype strains by various CTX phages under laboratory conditions are demonstrated in this report. We have established a plasmid-based CTX phage replication system that supports the replication of CTX-1, CTX-cla, CTX-2, and CTX-O139. The replication of CTX-2 from the tandem repeat of lysogenic CTX-2 in Wave 2 El Tor strains is also presented. El Tor biotype strains can be transduced by CTX phages in vitro by introducing a point mutation in toxT, the transcriptional activator of the tcp (toxin coregulated pilus) gene cluster and the cholera toxin gene. This mutation also increases the expression of cholera toxin in El Tor strains in a sample single-phase culture. Our results thus constitute experimental evidence of the genetic mechanism of the evolution of V. cholerae.Vibrio cholerae | cholera toxin | CTX phage | biotype

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Section: Discussionmentioning

confidence: 79%

Section: Methodsmentioning

confidence: 99%

Section: Ctx-2 Replication From the Tandem Repeat Of Lysogenic Ctx-2 Inmentioning

confidence: 99%

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Replication of Vibrio cholerae classical CTX phage

Kim

Lee

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…A wave 1 ET strain acquired a classical CTX-2 prophage that then recombined with the El Tor CTX-1 prophage, giving rise to the unique CTX-3 prophage. It is postulated that CTX-3 then naturally transduced into a new genetic background that lacked any CTX prophages, ultimately giving rise to the AET (6).…”

mentioning

confidence: 99%

Phenotypic Analysis Reveals that the 2010 Haiti Cholera Epidemic Is Linked to a Hypervirulent Strain

et al. 2016

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bVibrio cholerae O1 El Tor strains have been responsible for pandemic cholera since 1961. These strains have evolved over time, spreading globally in three separate waves. Wave 3 is caused by altered El Tor (AET) variant strains, which include the strain with the signature ctxB7 allele that was introduced in 2010 into Haiti, where it caused a devastating epidemic. In this study, we used phenotypic analysis to compare an early isolate from the Haiti epidemic to wave 1 El Tor isolates commonly used for research. It is demonstrated that the Haiti isolate has increased production of cholera toxin (CT) and hemolysin, increased motility, and a reduced ability to form biofilms. This strain also outcompetes common wave 1 El Tor isolates for colonization of infant mice, indicating that it has increased virulence. Monitoring of CT production and motility in additional wave 3 isolates revealed that this phenotypic variation likely evolved over time rather than in a single genetic event. Analysis of available whole-genome sequences and phylogenetic analyses suggested that increased virulence arose from positive selection for mutations found in known and putative regulatory genes, including hns and vieA, diguanylate cyclase genes, and genes belonging to the lysR and gntR regulatory families. Overall, the studies presented here revealed that V. cholerae virulence potential can evolve and that the currently prevalent wave 3 AET strains are both phenotypically distinct from and more virulent than many El Tor isolates.

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“…Flp normally works as a homotetramer; however, in case of recombination between half-sites and full sites, the synapses imply three recombinases (27). In the case of Flp, trimer recombination is possibly related to the fact that active sites are assembled in trans (28). In contrast, Xer recombinases cleave DNA in cis.…”

Section: Discussionmentioning

confidence: 99%

XerD-mediated FtsK-independent integration of TLCϕ into the Vibrio cholerae genome

Midonet

Das

Paly

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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As in most bacteria, topological problems arising from the circularity of the two Vibrio cholerae chromosomes, chrI and chrII, are resolved by the addition of a crossover at a specific site of each chromosome, dif, by two tyrosine recombinases, XerC and XerD. The reaction is under the control of a cell division protein, FtsK, which activates the formation of a Holliday Junction (HJ) intermediate by XerD catalysis that is resolved into product by XerC catalysis. Many plasmids and phages exploit Xer recombination for dimer resolution and for integration, respectively. In all cases so far described, they rely on an alternative recombination pathway in which XerC catalyzes the formation of a HJ independently of FtsK. This is notably the case for CTXϕ, the cholera toxin phage. Here, we show that in contrast, integration of TLCϕ, a toxin-linked cryptic satellite phage that is almost always found integrated at the chrI dif site before CTXϕ, depends on the formation of a HJ by XerD catalysis, which is then resolved by XerC catalysis. The reaction nevertheless escapes the normal cellular control exerted by FtsK on XerD. In addition, we show that the same reaction promotes the excision of TLCϕ, along with any CTXϕ copy present between dif and its left attachment site, providing a plausible mechanism for how chrI CTXϕ copies can be eliminated, as occurred in the second wave of the current cholera pandemic. cholera | site-specific DNA recombination | lysogenic conversion | chromosome segregation | lateral gene transfer

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Molecular Insights Into the Evolutionary Pathway of Vibrio cholerae O1 Atypical El Tor Variants

Cited by 40 publications

References 32 publications

Replication of Vibrio cholerae classical CTX phage

Replication of Vibrio cholerae classical CTX phage

Phenotypic Analysis Reveals that the 2010 Haiti Cholera Epidemic Is Linked to a Hypervirulent Strain

XerD-mediated FtsK-independent integration of TLCϕ into the Vibrio cholerae genome

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