Effect of bacterial host repair systems on the viability of hydroxylamine and methyl methanesulfonate treated T4 and lambda bacteriophages.

Survival of HA1 or MMS-treated T4 and lambda phages was estimated in bacterial cells differing in their ability to repair DNA. It has been found that the mismatch repair system of the bacterial host, which involves mutS mutR MutL uvrE and dam loci, does not excise, or does so to only a limited extent, the nonpaired bases from DNA of HA or MMS-treated phages. Mutation in polA, both in the polymerase as well as in the 5' leads to 3' exonuclease activity, have a small effect on survival of HA-treated phages, whereas mutation in the polymerase activity has a pronounced effect on survival of MMS-treated phages. There was a difference in the effect of polA mutations on survival of MMS-treated T4 and lambda phages; the survival of the former was less affected than the latter. Induction of SOS response has no effect on repair of HA and MMS-treated phages. Pretreatment of bacterial host (including the ada- mutant) with low doses of alkylating agents increases the survival of MMS (but not HA)-treated phages; pretreatment of bacteria with HA has no effect on survival of HA-treated phages. Three lines of evidence: the different inactivation rates of MMS-treated T4 and lambda phages, variation in the effect of polA mutations on survival of T4 and lambda phages, and a different level of adaptive response in ada- cells towards of MMS-treated T4 and lambda phages, suggest that the patterns of DNA methylation in T4 and lambda phages are different.