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Chapter 8 : Xer Site-Specific Recombination: Promoting Chromosome Segregation

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Abstract:

Xer site-specific recombination was discovered in 1984 through its role in converting multimers of ColE1-related multicopy plasmids to monomers and hence ensuring their stable inheritance within . Research on Xer recombination has been devoted to: (i) characterizing the recombination reaction at the molecular level; (ii) understanding how the system converts plasmid and chromosomal dimers to monomers (and not monomers to dimers); and (iii) understanding how Xer recombination at chromosomal is integrated into other aspects of DNA metabolism and processing during the bacterial cell cycle. This chapter focuses on those features of the Xer system that differentiate it from the related site-specific recombination systems, Cre-,λ Int-/, and Flp-. In cells containing circular chromosomes, chromosome dimers can arise by RecA-dependent homologous recombination between sister chromatids. Studies of Xer site-specific recombination have revealed new mechanistic details of the tyrosine recombinase mechanism. Uncovering the relationships between Xer recombination and chromosome segregation and how these relate to cell division, homologous recombination, and DNA replication is revealing the sophisticated methods that have evolved in bacteria to ensure the stable duplication and inheritance of the genetic material. The characterization of a strategy to ensure that Xer recombination at chromosomal is restricted to converting chromosome dimers present at cell division to monomers reveals one new way in which bacteria can process temporal and spatial information.

Citation: Barre F, Sherratt D. 2002. Xer Site-Specific Recombination: Promoting Chromosome Segregation, p 149-161. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch8

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Figures

Image of Figure 1.
Figure 1.

The site-specific recombination reaction. The XerC and XerD recombinases are represented by the white and grey C-shaped molecules, respectively, the N terminus lying on top of the DNA and the C terminus lying below. The DNA strands of each of the two recombination sites are represented by arrows pointing in the 5′ to 3′ direction. The strands of one of the sites are represented by thick lines, and the strands of the other site are represented by thin lines. Each site contains a black strand and a grey strand. Black strands are processed by XerC, and grey strands are processed by XerD. Note that the two synapsed sites are represented as being antiparallel because the black strands (and the grey strands) from the two sites run in opposite directions. Black and grey triangles indicate the positions of cutting and rejoining by the XerC and XerD recombinases, respectively. Active recombinases have an extended C-terminal tail. (i) synapsis; (ii) XerC strand exchange; (iii) HJ conformation change; (iv) XerD strand exchange; (v) synapsis breakage.

Citation: Barre F, Sherratt D. 2002. Xer Site-Specific Recombination: Promoting Chromosome Segregation, p 149-161. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch8
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Image of Figure 2.
Figure 2.

Topology of recombination on plasmid substrates. (A) The recombination products of and substrates have a defined topology. Plasmid DNA is represented by its two strands. The oriented core recombination sites are indicated by black triangles. (B) A model for synapsis at or XerC and XerD are represented as small grey and white circles, PepA molecules are shown as large black circles, and ArgRor P-ArcA (for and respectively) is shown as a medium-sized grey circle. The core recombination sites are shown in parallel, as indicated by the black arrows. (C) The reaction, from substrate (left) to product (right).

Citation: Barre F, Sherratt D. 2002. Xer Site-Specific Recombination: Promoting Chromosome Segregation, p 149-161. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch8
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Image of Figure 3.
Figure 3.

Dimer formation by homologous recombination. Chromosomal DNA is depicted by black and grey double strands. To differentiate the two sister chromatids arising by replication, one of the parental black strands is depicted by a thicker line. The origin of replication is shown as a black circle, and is represented by a black triangle. The thickness of the arrows follows the relative frequency of the events shown. HJs made by homologous recombination can be resolved to crossover or noncrossover events. Ruv-ABC (and RusA/RecG) preferentially resolves them to noncrossover events. However, crossover events still occur. Consequently, dimers are formed. The Xer recombination system ensures their conversion to monomers.

Citation: Barre F, Sherratt D. 2002. Xer Site-Specific Recombination: Promoting Chromosome Segregation, p 149-161. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch8
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Image of Figure 4.
Figure 4.

The activity zone. (A) The DAZ corresponds to ∼30 kb around the natural position of ( ). The Xer activity of sites away from their original position is represented on top of the drawing ( ). Various deletions (dashed lines) and inversions around are also shown. Their effect on activity is indicated on the right by a plus or a minus sign. The simplest explanation for these complicated data is that there are sequence elements all over the chromosome that point toward and that to be active, a site must be placed at the junction between those elements ( ). It is believed that those sequence elements are smaller than 8 bp (F. Cornet, unpublished data). (B) Map of the chromosome, showing the position of the and genes, the position of and and the position of two replication terminator sites. There is absolutely no link between timing and/or termination of replication and activity. Indeed, a strain carrying a large inversion of the chromosome (the inverted region is indicated with an arrow), displacing close to oriC, does not present with the classical filamentous phenotype of strains ( ). In this strain, replication of occurs rapidly after initiation, and termination of replication is outside the zone for competency of ( ).

Citation: Barre F, Sherratt D. 2002. Xer Site-Specific Recombination: Promoting Chromosome Segregation, p 149-161. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch8
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Image of Figure 5.
Figure 5.

A model for the regulation of Xer recombination at Just after initiation of replication, the two newly replicated origins (black circles) are segregated away from midcell. In contrast, the region (white triangles) stays close to midcell after replication. Just after being replicated, the sister sites can be synapsed by the Xer recombinases (grey and white circle). XerC catalyzes HJ formation, and in the absence of FtsK, resolves them back to substrate. Chromosome dimers block segregation, forcing septum closure around the synapsed sites. FtsK (black ellipses at midcell) can then activate the complete recombination reaction.

Citation: Barre F, Sherratt D. 2002. Xer Site-Specific Recombination: Promoting Chromosome Segregation, p 149-161. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch8
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