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Category: Clinical Microbiology
Xer Site-Specific Recombination: Promoting Vertical and Horizontal Transmission of Genetic Information, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555819217/9781555819200_Chap07-1.gif /docserver/preview/fulltext/10.1128/9781555819217/9781555819200_Chap07-2.gifAbstract:
It was Barbara McClintock who first described the problems of segregation arising from the circularity of chromosomes during her studies on maize variegation ( 1 ). The importance of this observation, which could have passed as a mere oddity at the time because of the linear nature of chromosomes in Eukaryota, was only realized after the demonstration of the circular nature of the Escherichia coli chromosome by François Jacob and Elie Wollman in the 1960s ( 2 ). Since then, the wealth of information gained by genomic studies has shown that circular chromosomes are the norm in Bacteria and Archaea.
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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 dif sites of 715 bacterial chromosomes. The XerC and XerD recognition sites are underlined. Double-stranded DNA sequence of V. cholerae dif1, dif2 and difG, of the core cer and psi 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.
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 dif activity zone corresponds to the region in which dif 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. dif sites are shown as red and black lines. The FtsK protein is drawn in blue.
Chromosome dimer resolution. (A) Dead-end FtsK-independent XerC pathway of recombination between dif sites. (B) Chromosome dimer resolution pathway. (C) Topological control of Xer recombination.
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 cer and psi multimer four-node catenanes. (C) The topological filter controls Xer catalysis for plasmid dimer resolution.
IMEX integration depends on little homology with dif. (A) Schematic of the integration/excision of mobile elements into the genome of their host. (B) IMEX integration generates a new dif 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
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.