RecG controls DNA amplification at double-strand breaks and arrested replication forks.
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.
Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, UK.
Benura
B
Azeroglu
Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, UK.
David R F
DRF
Leach
D000818:Animals; D001426:Bacterial Proteins / Q000378:metabolism; D053903:DNA Breaks, Double-Stranded; D004265:DNA Helicases / Q000378:metabolism; D004260:DNA Repair; D004261:DNA Replication; D004706:Endodeoxyribonucleases / Q000378:metabolism; D004926:Escherichia coli / Q000201:enzymology* / Q000378:metabolism; D029968:Escherichia coli Proteins / Q000378:metabolism*; D005784:Gene Amplification; D006801:Humans; D008954:Models, Biological; D055503:Protein Multimerization; D011995:Recombination, Genetic; D059767:Recombinational DNA Repair
D001426:Bacterial Proteins; D029968:Escherichia coli Proteins; C061260:RuvB protein, Bacteria; C069806:ruvC protein, E coli; C071446:RecG protein, E coli; D004706:Endodeoxyribonucleases; C071059:Holliday junction DNA helicase, E coli; D004265:DNA Helicases
DNA amplification; RecG; double-strand break repair