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Abstract
Replication fork reversal (RFR) is a reaction that takes place in Escherichia coli at replication forks arrested by the inactivation of a replication protein. Fork reversal involves the annealing of the leading and lagging strand ends; it results in the formation of a Holliday junction adjacent to DNA double-strand end, both of which are processed by recombination enzymes. In several replication mutants, replication fork reversal is catalysed by the RuvAB complex, originally characterized for its role in the last steps of homologous recombination, branch migration and resolution of Holliday junctions. We present here the isolation and characterization of ruvA and ruvB single mutants that are impaired for RFR at forks arrested by the inactivation of polymerase III, while they remain capable of homologous recombination. The positions of the mutations in the proteins and the genetic properties of the mutants suggest that the mutations affect DNA binding, RuvA–RuvB interaction and/or RuvB-helicase activity. These results show that a partial RuvA or RuvB defect affects primarily RFR, implying that RFR is a more demanding reaction than Holliday junction resolution.
Highlights
Chromosome replication is not a continuous process but can be impaired by obstacles or by the inactivation of a replication protein
Replication fork reversal (RFR) is a reaction that takes place in Escherichia coli at replication forks arrested by the inactivation of a replication protein
Fork reversal involves the annealing of the leading and lagging strand ends; it results in the formation of a Holliday junction adjacent to DNA double-strand end, both of which are processed by recombination enzymes
Summary
Chromosome replication is not a continuous process but can be impaired by obstacles or by the inactivation of a replication protein. Restart of inactivated replication forks while limiting DNA damage and DNA recombination is a crucial process. It is clear that a large diversity of enzymes will cooperate to rescue inactivated replication forks, depending on the cause of replication arrest. A large panel of different reactions can take place prior to restart, which are determined by the cause of replication inactivation (Michel et al, 2004; 2007). A second important point is that recombination proteins are involved in all the reactions that were observed to take place prior to replication restart. Recombination proteins act on their normal substrates, doublestrand DNA ends, single-strand DNA gaps or Holliday junctions (HJs), which are made at blocked forks, and they act directly on replication forks, catalysing specific novel reactions (Baharoglu et al, 2006)
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