Recombinational repair of alkylation lesions in phage T4. II. Ethyl methanesulfonate.
Treatment of bacteriophage T4 by ethyl methanesulfonate (EMS) caused more than a doubling in recombination between two rII markers. The functions of genes 47, 46, 32, 30, uvsX and y are known to be required for genetic recombination, and mutants defective in these genes were found to be more sensitive to inactivation by EMS than wild-type phage. This suggests that a recombinational pathway involving the products of these genes may be employed in repairing EMS induced lethal lesions. Genes 45 and denV are apparently not involved in recombination, and mutants defective in these genes were not EMS-sensitive. Gene 47, 46 and y mutants which were defective in the repair of EMS induced lethal lesions had no detectable deficiency in their ability to undergo EMS-induced mutation. This implies that recombinational repair of EMS lesions does not contribute substantially to EMS mutagenesis. The results obtained here with EMS are general similar to the results reported in the preceding paper with MNNG, suggesting that the lesions caused by both of these monofunctional alkylating agents may be eliminated by similar recombinational repair processes.
D000478:Alkylation; D003090:Coliphages / Q000187:drug effects* / Q000235:genetics; D004260:DNA Repair; D005020:Ethyl Methanesulfonate / Q000494:pharmacology*; D008698:Mesylates / Q000494:pharmacology*; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology; D009154:Mutation; D011995:Recombination, Genetic / Q000187:drug effects*
D008698:Mesylates; D008769:Methylnitronitrosoguanidine; D005020:Ethyl Methanesulfonate