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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 CTX[straight phi] 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-Kn[straight phi]1), which uses the morphogenesis genes of another filamentous phage (fs2[straight phi]) to form infectious TLC-Kn[straight phi]1 phage particles. The TLC-Kn[straight phi]1 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 CTX[straight phi]) 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-Kn[straight phi]1 genome restored a perfect dif site and normal morphology to V. cholerae wild-type and mutant strains with dif^sup -^ filamentation phenotypes. Furthermore, lysogeny of a dif^sup -^ non-toxigenic V. cholerae with TLC-Kn[straight phi]1 promoted its subsequent toxigenic conversion through integration of CTX[straight phi] 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. [PUBLICATION ABSTRACT]

Details

Title
Satellite phage TLC[straight phi] enables toxigenic conversion by CTX phage through dif site alteration
Author
Hassan, Faizule; Kamruzzaman, M; Mekalanos, John J; Faruque, Shah M
Pages
982-5
Section
LETTER
Publication year
2010
Publication date
Oct 21, 2010
Publisher
Nature Publishing Group
ISSN
00280836
e-ISSN
14764687
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
763129194
Copyright
Copyright Nature Publishing Group Oct 21, 2010