Effect of beta-propiolactone on bacteriophages and Salmonella typhimurium.

Low concentrations of β-propiolactone (BPL) inactivated Salmonella typhimurium strains and the bacteriophage P22. When ultraviolet light-sensitive ( hcr -) mutants, recombination-deficient ( rec -) mutants, and wild type were treated with 0.05% BPL, rec - mutants were inactivated drastically, hcr - mutants were inactivated very rapidly, and wild type were inactivated slowly. BPL induced the prophage P221 from wild type and hcr - mutants. However, no prophage induction from rec - mutants by BPL was observed. When BPL-damaged bacteriophage P22 was assayed simultaneously on hcr - mutants, rec - mutants, and wild type, it was found that survival of P22 on wild type was slightly higher than that on rec> - and hcr - mutants. This observation suggests that the BPL-damaged bacteriophage genome was repaired, presumably through the combined action of bacterial excision, bacterial recombination, and phage recombination enzymes. When a clear plaque-forming mutant ( c 2) of P22 phage was treated with BPL and assayed on hosts either lysogenic or nonlysogenic for P221b, c + plaques were observed among survivors on the P221b lysogen, whereas no c + plaques were found on the nonlysogens. No significant increase in c + plaques was found in survivors on P221b lysogens of the rec - strain. It is concluded that BPL acts directly on phage DNA and results in inactivation, repair, and recombination.