RecG controls DNA amplification at double-strand breaks and arrested replication forks

Benura Azeroglu, David R F Leach

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

DNA amplification is a powerful mutational mechanism that is a hallmark of cancer and drug resistance. It is therefore important to understand the fundamental pathways that cells employ to avoid over-replicating sections of their genomes. Recent studies demonstrate that, in the absence of RecG, DNA amplification is observed at sites of DNA double-strand break repair (DSBR) and of DNA replication arrest that are processed to generate double-strand ends. RecG also plays a role in stabilising joint molecules formed during DSBR. We propose that RecG prevents a previously unrecognised mechanism of DNA amplification that we call reverse-restart, which generates DNA double-strand ends from incorrect loading of the replicative helicase at D-loops formed by recombination, and at arrested replication forks.

Original languageEnglish
JournalFEBS Letters
DOIs
Publication statusPublished - 28 Feb 2017

Keywords / Materials (for Non-textual outputs)

  • Journal Article
  • Review

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