RecG Directs DNA Synthesis during Double-Strand Break Repair

• DOI: 10.1371/journal.pgen.1005799
• Publication Date: 2016-02-12T18:41:11Z
• Authors: Benura Azeroglu; Julia S. P. Mawer; Charlotte A. Cockram; Martin A. White; A. M. Mahedi Hasan; Milana Filatenkova; David R. F. Leach
• Keywords: Replication protein A; Origin recognition complex

Homologous recombination provides a mechanism of DNA double-strand break repair (DSBR) that requires an intact, homologous template for synthesis. When synthesis associated with DSBR is convergent, the broken strands are replaced and accurate. However, if divergent established, over-replication flanking may occur deleterious consequences. The RecG protein Escherichia coli helicase translocase can re-model 3-way 4-way structures such as replication forks Holliday junctions. primary role in live cells has remained elusive. Here we show that, absence RecG, attempted accompanied by at site induced chromosomal break. Furthermore, double-stand ends generated recG mutant sites known to block forks. These ends, also trigger characteristic this mutant, which explain terminus region chromosome. loss unwinding joint molecules previously observed RuvAB suppressed deficient PriA mutation (priA300), arguing action ensures bound correctly on D-loops direct rather than unwind molecules. This led us put forward revised model re-modelling branched intermediates plays fundamental directing thus maintaining genomic stability.