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Effect of ß-Propiolactone on Bacteriophages and Salmonella typhimurium¹

Fels Research Institute and Department of Microbiology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140

Low concentrations of ß-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 (c₂) 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.

¹ Supported in part by grants from the National Science Foundation (NSF-GB-8503), and USPHS (NIH-AI-06429 and NIH-CA-10439).

Received 7/ 1/69. Accepted 9/10/69.