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FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae

Unlike most bacteria, Vibrio cholerae harbors two distinct, nonhomologous circular chromosomes (chromosome I and II). Many features of chromosome II are plasmid-like, which raised questions concerning its chromosomal nature. Plasmid replication and segregation are generally not coordinated with the...

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Autores principales: Val, Marie-Eve, Kennedy, Sean P., Karoui, Meriem El, Bonné, Laetitia, Chevalier, Fabien, Barre, François-Xavier
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2533119/
https://www.ncbi.nlm.nih.gov/pubmed/18818731
http://dx.doi.org/10.1371/journal.pgen.1000201
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author Val, Marie-Eve
Kennedy, Sean P.
Karoui, Meriem El
Bonné, Laetitia
Chevalier, Fabien
Barre, François-Xavier
author_facet Val, Marie-Eve
Kennedy, Sean P.
Karoui, Meriem El
Bonné, Laetitia
Chevalier, Fabien
Barre, François-Xavier
author_sort Val, Marie-Eve
collection PubMed
description Unlike most bacteria, Vibrio cholerae harbors two distinct, nonhomologous circular chromosomes (chromosome I and II). Many features of chromosome II are plasmid-like, which raised questions concerning its chromosomal nature. Plasmid replication and segregation are generally not coordinated with the bacterial cell cycle, further calling into question the mechanisms ensuring the synchronous management of chromosome I and II. Maintenance of circular replicons requires the resolution of dimers created by homologous recombination events. In Escherichia coli, chromosome dimers are resolved by the addition of a crossover at a specific site, dif, by two tyrosine recombinases, XerC and XerD. The process is coordinated with cell division through the activity of a DNA translocase, FtsK. Many E. coli plasmids also use XerCD for dimer resolution. However, the process is FtsK-independent. The two chromosomes of the V. cholerae N16961 strain carry divergent dimer resolution sites, dif1 and dif2. Here, we show that V. cholerae FtsK controls the addition of a crossover at dif1 and dif2 by a common pair of Xer recombinases. In addition, we show that specific DNA motifs dictate its orientation of translocation, the distribution of these motifs on chromosome I and chromosome II supporting the idea that FtsK translocation serves to bring together the resolution sites carried by a dimer at the time of cell division. Taken together, these results suggest that the same FtsK-dependent mechanism coordinates dimer resolution with cell division for each of the two V. cholerae chromosomes. Chromosome II dimer resolution thus stands as a bona fide chromosomal process.
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spelling pubmed-25331192008-09-26 FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae Val, Marie-Eve Kennedy, Sean P. Karoui, Meriem El Bonné, Laetitia Chevalier, Fabien Barre, François-Xavier PLoS Genet Research Article Unlike most bacteria, Vibrio cholerae harbors two distinct, nonhomologous circular chromosomes (chromosome I and II). Many features of chromosome II are plasmid-like, which raised questions concerning its chromosomal nature. Plasmid replication and segregation are generally not coordinated with the bacterial cell cycle, further calling into question the mechanisms ensuring the synchronous management of chromosome I and II. Maintenance of circular replicons requires the resolution of dimers created by homologous recombination events. In Escherichia coli, chromosome dimers are resolved by the addition of a crossover at a specific site, dif, by two tyrosine recombinases, XerC and XerD. The process is coordinated with cell division through the activity of a DNA translocase, FtsK. Many E. coli plasmids also use XerCD for dimer resolution. However, the process is FtsK-independent. The two chromosomes of the V. cholerae N16961 strain carry divergent dimer resolution sites, dif1 and dif2. Here, we show that V. cholerae FtsK controls the addition of a crossover at dif1 and dif2 by a common pair of Xer recombinases. In addition, we show that specific DNA motifs dictate its orientation of translocation, the distribution of these motifs on chromosome I and chromosome II supporting the idea that FtsK translocation serves to bring together the resolution sites carried by a dimer at the time of cell division. Taken together, these results suggest that the same FtsK-dependent mechanism coordinates dimer resolution with cell division for each of the two V. cholerae chromosomes. Chromosome II dimer resolution thus stands as a bona fide chromosomal process. Public Library of Science 2008-09-26 /pmc/articles/PMC2533119/ /pubmed/18818731 http://dx.doi.org/10.1371/journal.pgen.1000201 Text en Val et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Val, Marie-Eve
Kennedy, Sean P.
Karoui, Meriem El
Bonné, Laetitia
Chevalier, Fabien
Barre, François-Xavier
FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae
title FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae
title_full FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae
title_fullStr FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae
title_full_unstemmed FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae
title_short FtsK-Dependent Dimer Resolution on Multiple Chromosomes in the Pathogen Vibrio cholerae
title_sort ftsk-dependent dimer resolution on multiple chromosomes in the pathogen vibrio cholerae
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2533119/
https://www.ncbi.nlm.nih.gov/pubmed/18818731
http://dx.doi.org/10.1371/journal.pgen.1000201
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