Document Type

Post-Print

Publication Date

5-15-2015

Subjects

DNA repair -- Molecular aspects, Chromosome replication -- Analysis, Mutation (Biology), Genomics

Abstract

Several aspects of the mechanism of homologous double strand break repair remain unclear. Although intensive efforts have focused on how recombination reactions initiate, far less is known about the molecular events that follow. Based upon biochemical studies, current models propose that RecBCD processes double strand ends and loads RecA to initiate recombinational repair. However, recent studies have shown that RecBCD plays a critical role in completing replication events on the chromosome through a mechanism that does not involve RecA or recombination. Here, we examine several studies, both early and recent, that suggest RecBCD also operates late in the recombination process- after initiation, strand invasion, and crossover resolution have occurred. Similar to its role in completing replication, we propose a model in which RecBCD is required to resect and resolve the DNA synthesis associated with homologous recombination at the point where the missing sequences on the broken molecule have been restored. We explain how the impaired ability to complete chromosome replication in recBC and recD mutants is likely to account for the loss of viability and genome instability in these mutants, and conclude that spontaneous double strand breaks and replication fork collapse occur far less frequently than previously speculated.

Description

NOTICE: this is the author’s version of a work that was accepted for publication in DNA Repair. Changes resulting from the publishing process. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published at: http://dx.doi.org/10.1016/j.dnarep.2015.04.018

© 2015, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/

Persistent Identifier

http://archives.pdx.edu/ds/psu/15291

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