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Satellite phage TLCφ enables toxigenic conversion by CTX phage through dif site alteration.

Hassan F, Kamruzzaman M, Mekalanos JJ, Faruque SM - Nature (2010)

Bottom Line: Bacterial cells defective in the dimer resolution often show an aberrant filamentous cell morphology.We found that acquisition and chromosomal integration of the TLC-Knφ1 genome restored a perfect dif site and normal morphology to V. cholerae wild-type and mutant strains with dif(-) filamentation phenotypes.Furthermore, lysogeny of a dif(-) non-toxigenic V. cholerae with TLC-Knφ1 promoted its subsequent toxigenic conversion through integration of CTXφ into the restored dif site.

View Article: PubMed Central - PubMed

Affiliation: Molecular Genetics Laboratory, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1212, Bangladesh.

ABSTRACT
Bacterial chromosomes often carry integrated genetic elements (for example plasmids, transposons, prophages and islands) whose precise function and contribution to the evolutionary fitness of the host bacterium are unknown. The CTXφ prophage, which encodes cholera toxin in Vibrio cholerae, is known to be adjacent to a chromosomally integrated element of unknown function termed the toxin-linked cryptic (TLC). Here we report the characterization of a TLC-related element that corresponds to the genome of a satellite filamentous phage (TLC-Knφ1), which uses the morphogenesis genes of another filamentous phage (fs2φ) to form infectious TLC-Knφ1 phage particles. The TLC-Knφ1 phage genome carries a sequence similar to the dif recombination sequence, which functions in chromosome dimer resolution using XerC and XerD recombinases. The dif sequence is also exploited by lysogenic filamentous phages (for example CTXφ) for chromosomal integration of their genomes. Bacterial cells defective in the dimer resolution often show an aberrant filamentous cell morphology. We found that acquisition and chromosomal integration of the TLC-Knφ1 genome restored a perfect dif site and normal morphology to V. cholerae wild-type and mutant strains with dif(-) filamentation phenotypes. Furthermore, lysogeny of a dif(-) non-toxigenic V. cholerae with TLC-Knφ1 promoted its subsequent toxigenic conversion through integration of CTXφ into the restored dif site. These results reveal a remarkable level of cooperative interactions between multiple filamentous phages in the emergence of the bacterial pathogen that causes cholera.

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Transduction with TLC-Knϕ1 phage cures cell filamentation of Vibrio cholerae O1 strains which have likely defects in resolution of chromosome dimers. Panels a through c (a,strain AO12682, b, strain AO7543, and c, strain AV2684248, see Table S1 and Table S4 for details) show the morphology of three different strains before infection with TLC-Knϕ1 whereas panels d through f show the same strains respectively after infection and chromosomal integration of TLC-Knϕ1.
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Figure 3: Transduction with TLC-Knϕ1 phage cures cell filamentation of Vibrio cholerae O1 strains which have likely defects in resolution of chromosome dimers. Panels a through c (a,strain AO12682, b, strain AO7543, and c, strain AV2684248, see Table S1 and Table S4 for details) show the morphology of three different strains before infection with TLC-Knϕ1 whereas panels d through f show the same strains respectively after infection and chromosomal integration of TLC-Knϕ1.

Mentions: Cultures of V. cholerae strains with deletions in the dif recombination site are known to contain a subpopulation of cells that display a filamentous morphology3. These filaments reflect aberrant cell division resulting from a defect in XerC/XerD-mediated chromosome dimer resolution3. We examined whether naturally occurring V. cholerae O1 strains that lack TLC, or the bona fide dif sequence, display filamentous morphology. As shown in Fig 3 and Table S3, these strains indeed display filamentous morphology for a noticeable sub-population of their cells. We next tested whether transduction with TLC-Knϕ1 phage could correct this morphology defect. In each case, cell filamentation in these V. cholerae was found to be eliminated following transduction with TLC-Knϕ1 (Fig. 3, Table S3). These results suggest that these filamentous strains are indeed dif-deficient and that lysogeny with TLC-Knϕ1 apparently corrected this defect.


Satellite phage TLCφ enables toxigenic conversion by CTX phage through dif site alteration.

Hassan F, Kamruzzaman M, Mekalanos JJ, Faruque SM - Nature (2010)

Transduction with TLC-Knϕ1 phage cures cell filamentation of Vibrio cholerae O1 strains which have likely defects in resolution of chromosome dimers. Panels a through c (a,strain AO12682, b, strain AO7543, and c, strain AV2684248, see Table S1 and Table S4 for details) show the morphology of three different strains before infection with TLC-Knϕ1 whereas panels d through f show the same strains respectively after infection and chromosomal integration of TLC-Knϕ1.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2967718&req=5

Figure 3: Transduction with TLC-Knϕ1 phage cures cell filamentation of Vibrio cholerae O1 strains which have likely defects in resolution of chromosome dimers. Panels a through c (a,strain AO12682, b, strain AO7543, and c, strain AV2684248, see Table S1 and Table S4 for details) show the morphology of three different strains before infection with TLC-Knϕ1 whereas panels d through f show the same strains respectively after infection and chromosomal integration of TLC-Knϕ1.
Mentions: Cultures of V. cholerae strains with deletions in the dif recombination site are known to contain a subpopulation of cells that display a filamentous morphology3. These filaments reflect aberrant cell division resulting from a defect in XerC/XerD-mediated chromosome dimer resolution3. We examined whether naturally occurring V. cholerae O1 strains that lack TLC, or the bona fide dif sequence, display filamentous morphology. As shown in Fig 3 and Table S3, these strains indeed display filamentous morphology for a noticeable sub-population of their cells. We next tested whether transduction with TLC-Knϕ1 phage could correct this morphology defect. In each case, cell filamentation in these V. cholerae was found to be eliminated following transduction with TLC-Knϕ1 (Fig. 3, Table S3). These results suggest that these filamentous strains are indeed dif-deficient and that lysogeny with TLC-Knϕ1 apparently corrected this defect.

Bottom Line: Bacterial cells defective in the dimer resolution often show an aberrant filamentous cell morphology.We found that acquisition and chromosomal integration of the TLC-Knφ1 genome restored a perfect dif site and normal morphology to V. cholerae wild-type and mutant strains with dif(-) filamentation phenotypes.Furthermore, lysogeny of a dif(-) non-toxigenic V. cholerae with TLC-Knφ1 promoted its subsequent toxigenic conversion through integration of CTXφ into the restored dif site.

View Article: PubMed Central - PubMed

Affiliation: Molecular Genetics Laboratory, International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka-1212, Bangladesh.

ABSTRACT
Bacterial chromosomes often carry integrated genetic elements (for example plasmids, transposons, prophages and islands) whose precise function and contribution to the evolutionary fitness of the host bacterium are unknown. The CTXφ prophage, which encodes cholera toxin in Vibrio cholerae, is known to be adjacent to a chromosomally integrated element of unknown function termed the toxin-linked cryptic (TLC). Here we report the characterization of a TLC-related element that corresponds to the genome of a satellite filamentous phage (TLC-Knφ1), which uses the morphogenesis genes of another filamentous phage (fs2φ) to form infectious TLC-Knφ1 phage particles. The TLC-Knφ1 phage genome carries a sequence similar to the dif recombination sequence, which functions in chromosome dimer resolution using XerC and XerD recombinases. The dif sequence is also exploited by lysogenic filamentous phages (for example CTXφ) for chromosomal integration of their genomes. Bacterial cells defective in the dimer resolution often show an aberrant filamentous cell morphology. We found that acquisition and chromosomal integration of the TLC-Knφ1 genome restored a perfect dif site and normal morphology to V. cholerae wild-type and mutant strains with dif(-) filamentation phenotypes. Furthermore, lysogeny of a dif(-) non-toxigenic V. cholerae with TLC-Knφ1 promoted its subsequent toxigenic conversion through integration of CTXφ into the restored dif site. These results reveal a remarkable level of cooperative interactions between multiple filamentous phages in the emergence of the bacterial pathogen that causes cholera.

Show MeSH
Related in: MedlinePlus