Ames strain TA100 was cured of its Fels 1 and Fels 2 prophages to yield the corresponding nonlysogenic derivative designated TAQ100. The two monolysogenic strains corresponding to TA100 lysogenic for Fels 1 (TAQ100F1) and for Fels 2 (TAQ100F2) were also isolated. In addition, the equivalent strains lacking pKM101 and designated TAQ1535, TAQ1535F1, and TAQ1535F2 were obtained. Ames strains TA98 and TA1 538 are lysogenic for Fels 2 and were observed by colony hybridization to contain cryptic Fels 1 DNA sequences. Strains corresponding to TA98 and TA1 538 cured of Fels 2 were isolated and designated TAQ98F1d and TAQ1538F1d, respectively.

Fels 1 grew poorly on Fels 1-cured strains, and Fels 2 grew not at all on Fels 2-cured strains. The cured strains had therefore to be identified as such by their failure to react in colony hybridization with 32P-labeled probes of Fels 1 and/or Fels 2 DNA. The specificity of the labeled probes was confirmed with the aid of the nonlysogenic Salmonella typhimurium strain Q1 and its two monolysogenic derivatives Q1 (Fels 1) and Q1 (Fels 2).

The cured strains were found to respond in the same manner as did the standard Ames strains to a variety of well-known mutagens, including aflatoxin B1, 7,12-dimethylbenz(a)anthracene, daunorubicin, 2-amino-dipyrido[1,2-a:3′,2′-d]imidazole, and β-naphthylamine. Also, mitomycin C, bleomycin, and diethylstilbestrol were nonmutagenic to TAQ100 and TAQ98F1 d as they are to TA100 and TA98. Since the Fels prophages are inducible by aflatoxin B1, by daunorubicin, and by other agents, it seems that mutagenesis and Fels prophage induction occur in separate subpopulations of cells; this situation had previously been reported to occur for mutagenesis and prophage γ induction in Escherichia coli. In any case, the Fels prophages appear to have no major influence on the mutagenic response of the Ames strains.

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This work was supported by the National Cancer Institute of Canada.

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