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Vol. 14, No. 23, pp. 2976-2988, December 1, 2000
1 Division of Molecular Genetics, Department of
Biochemistry, University of Oxford, OX1 3QU, UK;
2 Laboratoire de Microbiologie et Génétique
Moléculaire, Centre National de la Recherche Scientifique,
Toulouse, France
In bacteria with circular chromosomes, homologous recombination can
generate chromosome dimers that cannot be segregated to daughter cells
at cell division. Xer site-specific recombination at dif, a
28-bp site located in the replication terminus region of the
chromosome, converts dimers to monomers through the sequential action
of the XerC and XerD recombinases. Chromosome dimer resolution requires
that dif is positioned correctly in the chromosome, and the
activity of FtsK, a septum-located protein that coordinates cell
division with chromosome segregation. Here, we show that cycles of
XerC-mediated strand exchanges form and resolve Holliday junction
intermediates back to substrate irrespective of whether conditions
support a complete recombination reaction. The C-terminal domain of
FtsK is sufficient to activate the exchange of the second pair of
strands by XerD, allowing both intra- and intermolecular recombination
reactions to go to completion. Proper positioning of dif in the
chromosome and of FtsK at the septum is required to sense the
multimeric state of newly replicated chromosomes and restrict complete
Xer reactions to dimeric chromosomes.
[Key Words: Xer recombination; Holliday junction; chromosome segregation; FtsK]
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