Abstract

A high-frequency-transducing (HFT) lysate for tetracycline resistance ( tet R) was obtained by inducing an unusual tet R P22 lysogen which had been made by transducing Salmonclla typhimurium LT-2 to tet R with P22 phage grown on an LT-2 strain carrying the R factor 222. The HFT lystate contains defective P22 particles, called P22 Tc-10, which cannot grow or lysogenize (i.e., transduce tet R) upon single infection. However, two defective P22 Tc-10 particles can cooperate with each other for growth or for lysogeny (i.e., transduction of tet R), “Wild-type” phages which can grow on single infection and which no longer transduce tet R can be found at a frequency of 5 × 10 −5 PFU/particle in the HFT lysate. Five percent of these “wild-type” phages are also integration deficient. At high multiplicities of infection the tet R transductants made with an HFT lysate appear to be similar to a P22 Tc-10 lysogen (i.e., they are immune to P22 and yield HFT lysates upon induction); at low multiplicities of infection, many of the tet R transductants are tet R P22 prophage deletions. To account for these observations, a model is proposed in which the genes for tet R are inserted into the intact P22 genome in the P22 Tc-10 prophage. The consequences of such an insertion are discussed with regard to the structure of phage P22 DNA and the topological requirements for successful DNA replication, phage growth, and lysogenization.

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