Error-free recombinational repair predominates over mutagenic translesion replication in E-coli

Tolerance mechanisms are important in the ability of cells to cope with DNA damage. In E. coli, the two main damage tolerance mechanisms are recombinational repair (RR) and translesion replication (TLR). Here we show that FIR effectively repairs gaps opposite DNA lesions. When both mechanisms are functional, FIR predominates over TLR, being responsible for 86% of the repair events. This predominance of FIR is determined by the high concentration of RecA present under SOS conditions, which causes a differential inhibition of TLR. Further inhibition of TLR is caused by the RecA-catalyzed strand exchange reaction of FIR. This molecular hierarchy in the tolerance of DNA lesions ensures that the nonmutagenic FIR predominates over the mutagenic TLR, thereby contributing to genetic stability.