Recovery of DNA replication in UV-irradiated Escherichia coli requires both excision repair and RecF protein function

After UV doses that disrupt DNA replication, the recovery of replication at replication forks in Escherichia coli requires a functional copy of the re cF gene. In recF mutants, replication fails to recover and extensive degrad ation of the nascent DNA occurs, suggesting that recF function is needed to stabilize the disrupted replication forks and facilitate the process of re covery. We show here that the ability of recF to promote the recovery of re plication requires that the disrupting lesions be removed. In the absence o f excision repair, recF(+) cells protect the nascent DNA at replication for ks, but replication does not resume. The classical view is that recombinati on proteins operate in pathways that are independent from DNA repair, and t herefore the functions of Rec proteins have been studied in repair deficien t cells. However, mutations in either uvr or recF result in failure to reco ver replication at UV doses from which wild-type cells recover efficiently, suggesting that recF and excision repair contribute to a common pathway in the recovery of replication.