Chromosome Dimer Resolution

Abstract

This chapter presents the processes that can lead to the dimerization of replicons and discusses the mechanisms that ensure their resolution. It also discusses how chromosome dimer resolution is integrated into other aspects of DNA processing during the bacterial cell cycle. The chromosomes and linear plasmids of Borrelia are linear with hairpin ends. Bidirectional replication is initiated internally and, when complete, generates a circular dimer of the original linear replicon. In this circular dimer, the hairpin sites of the parental DNA are converted into palindromic “telomere” sites, which are used for chromosome dimer resolution. Xer site-specific recombination, which is responsible for chromosome dimer resolution, ensured their stable inheritance within Escherichia coli. In Borrelia and in bacteriophage N15 of E. coli, resolution of chromosome dimers is due to the action of a single enzyme, ResT or TelN, respectively. During tyrosine recombinase-mediated site-specific recombination, two tyrosine recombinase molecules bind cooperatively to ~30-bp specific core recombination sites in the DNA. The XerC and XerD site-specific recombinases function in chromosome dimer resolution by adding a single crossover at dif, a specific 28-bp core site located in the region of termination of replication of the chromosome. In vivo and in vitro studies show that in the absence of FtsK, Holliday junctions (HJs) are created and resolved back to the original substrate in cycles of XerC-mediated strand exchanges. The realization that Xer recombination uses different strategies to ensure resolution selectivity during plasmid and chromosome dimer resolution demonstrates the sophistication that has developed during bacterial evolution.