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Satellite phage TLCϕ enables toxigenic conversion by CTX phage through dif site alteration
Bacterial chromosomes often carry integrated genetic elements (e.g., 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 cholerae1, is known to b...
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Formato: | Texto |
Lenguaje: | English |
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2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967718/ https://www.ncbi.nlm.nih.gov/pubmed/20944629 http://dx.doi.org/10.1038/nature09469 |
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author | Hassan, Faizule Kamruzzaman, M. Mekalanos, John J. Faruque, Shah M. |
author_facet | Hassan, Faizule Kamruzzaman, M. Mekalanos, John J. Faruque, Shah M. |
author_sort | Hassan, Faizule |
collection | PubMed |
description | Bacterial chromosomes often carry integrated genetic elements (e.g., 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 cholerae1, is known to be adjacent to a chromosomally integrated element of unknown function termed the toxin-linked cryptic (TLC)2. Here we report 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 recombinases3. The dif sequence is also exploited by lysogenic filamentous phages (e.g., CTXϕ) for chromosomal integration of their genomes. Bacterial cells defective in the dimer resolution often show an aberrant filamentous cell morphology3,4. 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 that displayed dif(-) filamentation phenotypes. Furthermore, lysogeny of a dif(-) nontoxigenic 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. |
format | Text |
id | pubmed-2967718 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
record_format | MEDLINE/PubMed |
spelling | pubmed-29677182011-04-21 Satellite phage TLCϕ enables toxigenic conversion by CTX phage through dif site alteration Hassan, Faizule Kamruzzaman, M. Mekalanos, John J. Faruque, Shah M. Nature Article Bacterial chromosomes often carry integrated genetic elements (e.g., 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 cholerae1, is known to be adjacent to a chromosomally integrated element of unknown function termed the toxin-linked cryptic (TLC)2. Here we report 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 recombinases3. The dif sequence is also exploited by lysogenic filamentous phages (e.g., CTXϕ) for chromosomal integration of their genomes. Bacterial cells defective in the dimer resolution often show an aberrant filamentous cell morphology3,4. 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 that displayed dif(-) filamentation phenotypes. Furthermore, lysogeny of a dif(-) nontoxigenic 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. 2010-10-13 2010-10-21 /pmc/articles/PMC2967718/ /pubmed/20944629 http://dx.doi.org/10.1038/nature09469 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article Hassan, Faizule Kamruzzaman, M. Mekalanos, John J. Faruque, Shah M. Satellite phage TLCϕ enables toxigenic conversion by CTX phage through dif site alteration |
title | Satellite phage TLCϕ enables toxigenic conversion by CTX phage through dif site alteration |
title_full | Satellite phage TLCϕ enables toxigenic conversion by CTX phage through dif site alteration |
title_fullStr | Satellite phage TLCϕ enables toxigenic conversion by CTX phage through dif site alteration |
title_full_unstemmed | Satellite phage TLCϕ enables toxigenic conversion by CTX phage through dif site alteration |
title_short | Satellite phage TLCϕ enables toxigenic conversion by CTX phage through dif site alteration |
title_sort | satellite phage tlcϕ enables toxigenic conversion by ctx phage through dif site alteration |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967718/ https://www.ncbi.nlm.nih.gov/pubmed/20944629 http://dx.doi.org/10.1038/nature09469 |
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