作者: Lior Izhar , Moshe Goldsmith , Ronny Dahan , Nicholas Geacintov , Robert G. Lloyd
DOI: 10.1016/J.JMB.2008.06.031
关键词:
摘要: Daughter strand gaps formed upon interruption of replication at DNA lesions in Escherichia coli can be repaired by either translesion synthesis or homologous recombination (HR) repair. Using a plasmid-based assay system that enables discrimination between transfer and template switching (information copying) modes HR gap repair, we found approximately 80% were physical from the donor, whereas 20% appear to switching. repair operated on both small bulky largely depended RecA RecF but not RecBCD nuclease. In addition, was mildly reduced cells lacking RuvABC RecG proteins involved resolution Holliday junctions. These results, obtained for first time under conditions detect two mechanisms, provide vivo high-resolution molecular evidence predominance mechanism A significant portion appears occur via mechanism.