Mutants carrying recF143 or recF144 show wild type levels of host cell reactivation of UV-irradiated lambdavir and wild type rates of excision gap closure in repairing UV damage to their own DNA. The same mutants showed reduced rates of postreplication repair strand joining. When uvrA- recF- or uvrB- recF- strains are tested, postreplication repair strand joining is incomplete or does not occur at fluences above 1 J/m2. We suggest that there may be a UvrAB and a RecF pathway of postreplication repair or that the repair functions controlled or determined by uvrA uvrB and by recF may be similar. An intermediate in postreplication repair may accumulate in the uvr- recF- strain.