In order to clarify more definitely and quantitatively the relationship between host-controlled variation and multiplicity activation (Toyama et al., 1962), proportions of plaque formers to phage-infected cells were determined at various m. o. i. (multiplicity of infection) in infection of cells of Salmonella butantan (=I-1) with phage ε
15 propagated on cells of Salmonella anatum (=A), and vice versa. Theoretical proportions were also calculated, under the assumption that each cell may become a plaque former when it receives 2. 3, 4, 5 and/or 6 phage particles or more, and compared to the data observed.
The results showed clearly that cells of I-1, which do not allow multiplication of phage ε
15 propagated on cells of A when singly infected, may allow phage multiplication when multiply infected. Similar phenomenon was also observed in infection of cells A with phage ε
15 propagated on cells of I-1, however, in this case, very high m. o. i. was required for phage multiplication and the effect of multiplicity activation was to a lesser extent than that observed in the former case.
ε
15ts is a mutant of ε
15, incapable of reproducing at 37°C while capable at 25°C. Phages ε
15ts[A] are capable of contributing to multiplicity activation in infection of cells I-1 with phage ε
15 ts vir [A] whereas phages ε
15ts[I-1] are incapable, indicating that the helper effect of ε
15ts[A] is attributed to nongenetic multiplicity activation but not to marker rescue due to genetic recombination.
When inactivated by ultraviolet light irradiation to ca. 10
-5 survival, phages ε
15[A] are no longer capable of contributing to multiplicity activation in infection of I-1 with ε
15ts+vir[A].
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