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FtsK-dependent dimer resolution on multiple chromosomes in the pathogen Vibrio cholerae.

Val ME, Kennedy SP, El Karoui M, Bonné L, Chevalier F, Barre FX - PLoS Genet. (2008)

Bottom Line: However, the process is FtsK-independent.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.Chromosome II dimer resolution thus stands as a bona fide chromosomal process.

View Article: PubMed Central - PubMed

Affiliation: CNRS, Centre de Génétique Moléculaire, UPR 2167, Gif-sur-Yvette, France.

ABSTRACT
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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The non-homologous chromosomes of Proteobacteria with multipartite genomes carry divergent dif sites.Alignment of the chromosome dimer resolution sites of a few Proteobacteria harboring a single or multiple chromosomes. Bases identical to the γ-Proteobacteria dif consensus are shaded in black. Species abbreviations follow the KEGG convention.
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pgen-1000201-g007: The non-homologous chromosomes of Proteobacteria with multipartite genomes carry divergent dif sites.Alignment of the chromosome dimer resolution sites of a few Proteobacteria harboring a single or multiple chromosomes. Bases identical to the γ-Proteobacteria dif consensus are shaded in black. Species abbreviations follow the KEGG convention.

Mentions: Putative dif sites were readily identified on each of the two chromosomes harbored by 7 additional γ-Proteobacteria (Figure 7 and Figure S2). To determine dif sites in β- and α-Proteobacteria, we generated a profile Hidden Markov Model (HMM) based on the alignment of the putative CDR sites found in the larger chromosome of 27 γ-Proteobacteria using the program HHMER. We then compared each sequence by hand to ensure the proper 6 bp spacing between the putative XerC and XerD binding sites. Putative dif sites were thus identified on each of the multiple chromosomes harbored by 10 β-Proteobacteria species and 5 α-Proteobacteria species (Figure 7 and Figure S3 and S4). A single pair of recombinases orthologous to XerC and XerD was found in each of the 22 additional γ-, β- and α-Proteobacteria harboring multiple chromosomes, suggesting that a single pair of recombinases ensures dimer resolution of each of their non-homologous chromosomes. FtsK orthologues were also found. In addition, putative dif sites fell within 10 kb of the GC-skew inflection point (data not shown), suggesting that dimer resolution is under the control of an FtsK-like homologue in all these species. Thus, the adoption of an FtsK-dependent dimer resolution system could be a key evolutionary step in the maintenance of large circular replicons.


FtsK-dependent dimer resolution on multiple chromosomes in the pathogen Vibrio cholerae.

Val ME, Kennedy SP, El Karoui M, Bonné L, Chevalier F, Barre FX - PLoS Genet. (2008)

The non-homologous chromosomes of Proteobacteria with multipartite genomes carry divergent dif sites.Alignment of the chromosome dimer resolution sites of a few Proteobacteria harboring a single or multiple chromosomes. Bases identical to the γ-Proteobacteria dif consensus are shaded in black. Species abbreviations follow the KEGG convention.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2533119&req=5

pgen-1000201-g007: The non-homologous chromosomes of Proteobacteria with multipartite genomes carry divergent dif sites.Alignment of the chromosome dimer resolution sites of a few Proteobacteria harboring a single or multiple chromosomes. Bases identical to the γ-Proteobacteria dif consensus are shaded in black. Species abbreviations follow the KEGG convention.
Mentions: Putative dif sites were readily identified on each of the two chromosomes harbored by 7 additional γ-Proteobacteria (Figure 7 and Figure S2). To determine dif sites in β- and α-Proteobacteria, we generated a profile Hidden Markov Model (HMM) based on the alignment of the putative CDR sites found in the larger chromosome of 27 γ-Proteobacteria using the program HHMER. We then compared each sequence by hand to ensure the proper 6 bp spacing between the putative XerC and XerD binding sites. Putative dif sites were thus identified on each of the multiple chromosomes harbored by 10 β-Proteobacteria species and 5 α-Proteobacteria species (Figure 7 and Figure S3 and S4). A single pair of recombinases orthologous to XerC and XerD was found in each of the 22 additional γ-, β- and α-Proteobacteria harboring multiple chromosomes, suggesting that a single pair of recombinases ensures dimer resolution of each of their non-homologous chromosomes. FtsK orthologues were also found. In addition, putative dif sites fell within 10 kb of the GC-skew inflection point (data not shown), suggesting that dimer resolution is under the control of an FtsK-like homologue in all these species. Thus, the adoption of an FtsK-dependent dimer resolution system could be a key evolutionary step in the maintenance of large circular replicons.

Bottom Line: However, the process is FtsK-independent.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.Chromosome II dimer resolution thus stands as a bona fide chromosomal process.

View Article: PubMed Central - PubMed

Affiliation: CNRS, Centre de Génétique Moléculaire, UPR 2167, Gif-sur-Yvette, France.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus