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Xer Site-Specific Recombination: Promoting Vertical and Horizontal Transmission of Genetic Information

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  • Authors: Caroline Midonet1, Francois-Xavier Barre2
  • Editors: Phoebe Rice3, Nancy Craig4
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Institute for Integrative Biology of the Cell (I2BC), Université Paris Saclay, CEA, CNRS, Université Paris Sud, 1 avenue de la Terrasse, 91198 Gif sur Yvette, France; 2: Institute for Integrative Biology of the Cell (I2BC), Université Paris Saclay, CEA, CNRS, Université Paris Sud, 1 avenue de la Terrasse, 91198 Gif sur Yvette, France; 3: University of Chicago, Chicago, IL; 4: Johns Hopkins University, Baltimore, MD
  • Source: microbiolspec December 2014 vol. 2 no. 6 doi:10.1128/microbiolspec.MDNA3-0056-2014
  • Received 09 October 2014 Accepted 10 October 2014 Published 12 December 2014
  • François-Xavier Barre, barre@cgm.cnrs-gif.fr
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  • Abstract:

    Two related tyrosine recombinases, XerC and XerD, are encoded in the genome of most bacteria where they serve to resolve dimers of circular chromosomes by the addition of a crossover at a specific site, . From a structural and biochemical point of view they belong to the Cre resolvase family of tyrosine recombinases. Correspondingly, they are exploited for the resolution of multimers of numerous plasmids. In addition, they are exploited by mobile DNA elements to integrate into the genome of their host. Exploitation of Xer is likely to be advantageous to mobile elements because the conservation of the Xer recombinases and of the sequence of their chromosomal target should permit a quite easy extension of their host range. However, it requires means to overcome the cellular mechanisms that normally restrict recombination to sites harbored by a chromosome dimer and, in the case of integrative mobile elements, to convert dedicated tyrosine resolvases into integrases.

  • Citation: Midonet C, Barre F. 2014. Xer Site-Specific Recombination: Promoting Vertical and Horizontal Transmission of Genetic Information. Microbiol Spectrum 2(6):MDNA3-0056-2014. doi:10.1128/microbiolspec.MDNA3-0056-2014.

Key Concept Ranking

Mobile Genetic Elements
0.49615288
0.49615288

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/content/journal/microbiolspec/10.1128/microbiolspec.MDNA3-0056-2014
2014-12-12
2017-11-23

Abstract:

Two related tyrosine recombinases, XerC and XerD, are encoded in the genome of most bacteria where they serve to resolve dimers of circular chromosomes by the addition of a crossover at a specific site, . From a structural and biochemical point of view they belong to the Cre resolvase family of tyrosine recombinases. Correspondingly, they are exploited for the resolution of multimers of numerous plasmids. In addition, they are exploited by mobile DNA elements to integrate into the genome of their host. Exploitation of Xer is likely to be advantageous to mobile elements because the conservation of the Xer recombinases and of the sequence of their chromosomal target should permit a quite easy extension of their host range. However, it requires means to overcome the cellular mechanisms that normally restrict recombination to sites harbored by a chromosome dimer and, in the case of integrative mobile elements, to convert dedicated tyrosine resolvases into integrases.

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FIGURE 1

Chromosome dimer resolution and sister chromosome decatenation. (A) Topological maintenance of bacterial chromosomes. Violet and pink circles represent sister circular chromosomes. Topo IV resolves catenanes. The Xer machinery resolves both catenanes and dimers. (B) Xer recombination. Light and dark grey ovoid shapes depict the C-terminal domains of the XerC and XerD tyrosine recombinases, respectively. The N-terminal domains are omitted for clarity. Tails have been added to indicate the C-terminal interactions of the recombinases. Red and black lines indicate the two strands of the recombining sites. Full and empty circles represent the XerC and XerD cleavage points, respectively. Horizontal and vertical substrates are proficient for XerC and XerD-strand exchanges, respectively. (C) Consensus sequence obtained from the alignment of the sites of 715 bacterial chromosomes. The XerC and XerD recognition sites are underlined. Double-stranded DNA sequence of and , of the core and plasmid sites and of the three types of attachment sites observed in the genome of integrative mobile elements exploiting Xer are shown below (ET: El Tor CTX; VGJ: VGJ phage; TLC: TLC satellite phage). XerC and XerD process the top and bottom strands, respectively. Bases differing from the consensus are shown in red. Lower case letters indicate the absence of conventional Watson–Crick pairing interactions. doi:10.1128/microbiolspec.MDNA3-0056-2014.f1

Source: microbiolspec December 2014 vol. 2 no. 6 doi:10.1128/microbiolspec.MDNA3-0056-2014
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FIGURE 2

Spatial and temporal control of chromosome dimer resolution. (A) Temporal restriction of Xer recombination during the bacterial cell cycle. White disk: origin of replication region; Converging arrows: terminus of replication region. The two sister chromatids are depicted as pink and purple tubes. (B) Spatial restriction of Xer recombination along bacterial chromosomes. The activity zone corresponds to the region in which can still resolve dimers if displaced. (C) FtsK controls Xer recombination. Violet and pink circles represent bacterial sister circular chromosomes. White arrows indicate the KOPS motifs and their orientation. sites are shown as red and black lines. The FtsK protein is drawn in blue. doi:10.1128/microbiolspec.MDNA3-0056-2014.f2

Source: microbiolspec December 2014 vol. 2 no. 6 doi:10.1128/microbiolspec.MDNA3-0056-2014
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FIGURE 3

Chromosome dimer resolution. (A) Dead-end FtsK-independent XerC pathway of recombination between sites. (B) Chromosome dimer resolution pathway. (C) Topological control of Xer recombination. doi:10.1128/microbiolspec.MDNA3-0056-2014.f3

Source: microbiolspec December 2014 vol. 2 no. 6 doi:10.1128/microbiolspec.MDNA3-0056-2014
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FIGURE 4

Plasmid dimer resolution. (A) Schematic representation of the topological filter. Yellow circles represent accessory proteins. P: PepA; A: ArgR or phosphorylated ArcA; Green tubes: accessory sequences. (B) Topology of the products of Xer recombination at and multimer four-node catenanes. (C) The topological filter controls Xer catalysis for plasmid dimer resolution. doi:10.1128/microbiolspec.MDNA3-0056-2014.f4

Source: microbiolspec December 2014 vol. 2 no. 6 doi:10.1128/microbiolspec.MDNA3-0056-2014
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FIGURE 5

IMEX integration depends on little homology with . (A) Schematic of the integration/excision of mobile elements into the genome of their host. (B) IMEX integration generates a new site, which allows for multiple successive integration events. (C) IMEX integration depends on limited homology. The distance separating the two bases of a base pair indicates the quality of the base pair interactions that are formed. N.D.: not determined doi:10.1128/microbiolspec.MDNA3-0056-2014.f5

Source: microbiolspec December 2014 vol. 2 no. 6 doi:10.1128/microbiolspec.MDNA3-0056-2014
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FIGURE 6

Diversity of the IMEX integration pathways. (A) Irreversible integration of CTX-type elements. The single-stranded DNA and double-stranded DNA forms of the element are represented in pink. The host genome is shown in purple. The incapacity of XerD to perform strand exchanges is indicated in yellow. Orange hexagons labeled with the letter E are EndoIII. (B) Integration/excision of VGJ-type elements. The double-stranded DNA replicative form of the element is shown in pink. The host genome is shown in purple. A yellow explosion indicates the impossibility for XerD to perform strand exchanges. The orange circle labeled with a question mark indicates a putative unknown integration factor. (C) Integration/excision pathway of TLC-type elements. The double-stranded DNA form of the element is shown in pink. The host genome is shown in purple. The Blue circle labeled with a question mark represents an unknown factor that could permit the binding of XerD and its catalytic activation. doi:10.1128/microbiolspec.MDNA3-0056-2014.f6

Source: microbiolspec December 2014 vol. 2 no. 6 doi:10.1128/microbiolspec.MDNA3-0056-2014
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