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Interference with the in vitro binding of lambda phage repressor to lambda operator DNA was observed when Escherichia coli DNA containing the following lesions was present in the reaction mixture: (a) DNA with single-strand breaks from pancreatic DNase (nicked DNA); (B) DNA isolated from thymine-straved cells; (c) DNA from ultraviolet-treated cells; (d) DNA of mitomycin-treated cells; and (e) DNA from a temperature-sensitive ligase mutant after 1 hr at 42 degrees. Normal E. coli DNA did not interfere. Binding of lambda cIing-minus repressor to operator DNA was not affected by E. coli DNA with lesions. DNAs from cells treated with increasing doses of mitomycin were proportionately more effective in competition for repressor, suggesting increasing binding sites per unit of DNA. A general model of virus induction is proposed, based on binding affinity of ultraviolet-sensitive repressors for single-strand breaks in the host DNA. The model is extended also to the presumptive repressor of cell division.

Proposed mechanism of bacteriophage lambda induction: acquisition of binding sites for lambda repressor by DNA of the host.