RecBCD coordinates repair of two ends at a DNA double-strand break, preventing aberrant chromosome amplification

Martin A. White, Benura Azeroglu, Manuel A. Lopez-Vernaza, A. M. Mahedi Hasan, David R. F. Leach

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

DNA double-strand break (DSB) repair is critical for cell survival. A diverse range of organisms from bacteria to humans rely on homologous recombination for accurate DSB repair. This requires both coordinate action of the two ends of a DSB and stringent control of the resultant DNA replication to prevent unwarranted DNA amplification and aneuploidy. In Escherichia coli, RecBCD enzyme is responsible for the initial steps of homologous recombination. Previous work has revealed recD mutants to be nuclease defective but recombination proficient. Despite this proficiency, we show here that a recD null mutant is defective for the repair of a two-ended DSB and that this defect is associated with unregulated chromosome amplification and defective chromosome segregation. Our results demonstrate that RecBCD plays an important role in avoiding this amplification by coordinating the two recombining ends in a manner that prevents divergent replication forks progressing away from the DSB site.
Original languageEnglish
Pages (from-to)6670-6682
Number of pages13
JournalNucleic Acids Research
Volume46
Issue number13
Early online date13 Jun 2018
DOIs
Publication statusPublished - 27 Jul 2018

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