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

• Luisa Laureti ^[1] ; Lara Lee ^[1] ; Gaëlle Philippin ^[1] ; Vincent Pagès ^[1]
  1. [1] Team DNA Damage Tolerance, Cancer Research Center of Marseille, CRCM, Aix Marseille univ, CNRS, inserm, institut Paoli-Calmettes, 13009 Marseille, France
• Localización: Nucleic acids research, ISSN 0305-1048, Vol. 45, Nº. 10, 2017, págs. 5877-5886
• Idioma: inglés
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• Resumen

  • The RecBCD complex is a key factor in DNA metabolism. This protein complex harbors a processive nuclease and two helicases activities that give it the ability to process duplex DNA ends. These enzymatic activities make RecBCD a major player in double strand break repair, conjugational recombination 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 recombinational repair of the gap and efficient translesion 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.