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  • The EMBO Journal (2006) 25, 5754 - 5763
  • doi:10.1038/sj.emboj.7601474

Published online: 30 November 2006

RecFOR proteins are essential for Pol V-mediated translesion synthesis and mutagenesis

Shingo Fujiia, Asako Isogawaa and Robert P Fuchs

  1. Genome Instability and Carcinogenesis, CNRS FRE2931, Marseille, France

Correspondence to:

Robert P Fuchs, Genome Instability and Carcinogenesis, CRNS, FRE 2931, 31, chemin Joseph Aiguier, 13402 Marseille cedex 20, 13402, France. Tel.: +33 4 9116 4271; Fax: +33 4 9116 4168; E-mail: fuchs@ibsm.cnrs-mrs.fr

aThese authors contributed equally to this work

Received 25 July 2006; Accepted 26 October 2006

When the replication fork moves through the template DNA containing lesions, daughter-strand gaps are formed opposite lesion sites. These gaps are subsequently filled-in either by translesion synthesis (TLS) or by homologous recombination. RecA filaments formed within these gaps are key intermediates for both of the gap-filling pathways. For instance, Pol V, the major lesion bypass polymerase in Escherichia coli, requires a functional interaction with the tip of the RecA filament. Here, we show that all three recombination mediator proteins RecFOR are needed to build a functionally competent RecA filament that supports efficient Pol V-mediated TLS in the presence of ssDNA-binding protein (SSB). A positive contribution of RecF protein to Pol V lesion bypass is demonstrated. When Pol III and Pol V are both present, Pol III imparts a negative effect on Pol V-mediated lesion bypass that is counteracted by the combined action of RecFOR and SSB. Mutations in recF, recO or recR gene abolish induced mutagenesis in E. coli.

  • Keywords:

    • competition between Pol III and Pol V,
    • induced mutagenesis,
    • Pol V-mediated lesion bypass,
    • RecFOR functions