Tandem repeat recombination induced by replication fork defects in Escherichia coli requires a novel factor, RadC

DnaB is the helicase associated with the DNA polymerase III replication for k in Escherichia coli. Previously we observed that the dnaB107(ts) mutation , at its permissive temperature, greatly stimulated deletion events at chro mosomal tandem repeats. This stimulation required recA, which suggests a re combinational mechanism. In this article we examine the genetic dependence of recombination stimulated by the dnaB107 mutation. Gap repair genes recF, recO and recR were not required. Mutations in recB, required for double-st rand break repair, and in ruvC, the Holliday junction resolvase gene, were synthetically lethal with dnaB107, causing enhanced temperature sensitivity . The hyperdeletion phenotype of dnaB107 was semidominant, and in dnaB107/d naB(+) heterozygotes recB was partially required for enhanced deletion, whe reas ruvC was not. We believe that dnaB107 causes the stalling of replicati on forks, which may become broken and require repair. Misalignment of repea ted sequences during RecBCD-mediated repair may account for most, but not a ll, of deletion stimulated by dnaB107 To our surprise, the radC gene, like recA, was required for virtually all recombination stimulated by dnaB107. T he biochemical function of RadC is unknown, but is reported to be required for growth-medium-dependent repair of DNA strand breaks. Our results sugges t that RadC functions specifically in recombinational repair that is associ ated with the replication fork.