A non-catalytic role of RecBCD in homology directed gap repair and translesion synthesis

The RecBCD complex is a key factor in DNA metabolism. This protein complex harbors a proces-sive nuclease and two helicases activities that give it the ability to process duplex DNA ends. These en-zymatic activities make RecBCD a major player in double strand break repair, conjugational recombi-nation and degradation of linear DNA. In this work, we unravel a new role of the RecBCD complex in the processing of DNA single-strand gaps that are generated at DNA replication-blocking lesions. We show that independently of its nuclease or helicase activities , the entire RecBCD complex is required for re-combinational repair of the gap and efficient transle-sion synthesis. Since none of the catalytic functions of RecBCD are required for those processes, we surmise that the complex acts as a structural element that stabilizes the blocked replication fork, allowing efficient DNA damage tolerance.