Abstract
As a result of the work of many laboratories, a new paradigm describing the manner by which bacteria respond to repair DNA damage has emerged. This paradigm holds that under any growth condition, essentially all replication forks formed at oriC encounter DNA damage and either stall or collapse before they can complete synthesis of the genome. Maintenance of cell viability therefore requires both correction of the DNA lesion via the action of the DNA repair enzymes and replication fork restart via the combined action of the DNA recombination and replication enzymes. A proposal has been advanced to distinguish this pathway, which operates as a housekeeping function in the absence of exogenous insult to the cell and is likely to be inherently nonmutagenic, from the SOS response, which is induced by exogenous DNA damage and includes error-prone repair, that it be named CPR for coordinated processing of damaged replication forks (M. M. Cox, M. F. Goodman, K. N. Kreuzer, D. J. Sherratt, S. J. Sandler, and K. J. Marians, submitted for publication). In this minireview, we will describe the central role of PriA in the replication fork restart step of CPR.
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