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- W2046989979 abstract "Abstract In heavily P32-labeled phage particles, plaque formation and abortive transduction activities are inactivated at similar exponential rates. The rate of inactivation of abortive transduction is uninfluenced by the recipient utilized in the transduction assay (single-site or multi-site mutations) or by preadsorption to, and subsequent growth of, recipient bacteria. It is concluded that P32-inactivating lesions are almost exclusively confined to the DNA and simultaneously inactivate the functioning of the entire genetic element or inactivate the ability of the genetic material to be carried by recipient bacteria in functional form. Abortive transducing elements are considered to be comprised of double-stranded DNA and to be transferred as completely conservative units during the duplication of recipient bacteria. The formation of complete transductional clones is exponentially inactivated in P32-labeled free particles at 0.08 to 0.2 the rate of inactivation of plaque formation. Like abortive transducing elements, those involved in complete transduction are inactivated at rates uninfluenced by the recipient (single-site or multi-site mutations) utilized in the assay. During P32 decay, no appreciable changes occur in the frequency of joint transduction of two linked markers. Complete transductions are inactivated with approximately single-hit kinetics; thus P32 lesions do not appear to “convert” abortively transducing elements into ones capable of complete transduction. It is concluded further that P32 lesions do not have as their prominent inactivating effect a permanently incapacitating damage to the bacterial genes actually incorporated to engender the wild-type recombinant, but rather affect gene function and the recombination process in some more indirect manner." @default.
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- W2046989979 date "1962-06-01" @default.
- W2046989979 modified "2023-09-27" @default.
- W2046989979 title "Effects of P32 decay on transduction by Salmonella phage P22" @default.
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- W2046989979 doi "https://doi.org/10.1016/0042-6822(62)90113-7" @default.
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