A mutant of 32, defective for deoxythymidine kinase (ATP: thymidine 5′-phosphotransferase EC and therefore unable to incorporate thymidine into DNA has been used to study alterations in thymidine utilization resulting from phage infection. Infection by the T-even phages leads to the rapid incorporation of [H]-thymidine into DNA which results from the induction of deoxythymidine kinase activity as first reported by Hiraga, Igarashi & Yura (1967). No effect was observed following infection of 32 by phages T3, T7, λ, Pl and Mu-1. The T4-induced enzyme differs from the wild-type cell enzyme in several properties including heat stability, deoxycytidine triphosphate stimulation and pH optimum and the ability to induce deoxythymidine kinase can be lost by mutation in a T4 gene () linked to I. T4 mutant-infected 32 cells fail to incorporate [H]-thymidine or 5-bromodeoxyuridine into DNA and the latter property formed the basis for the selection of the phage mutants. The T4 gene is non-essential for growth both in wild type and mutant cells since deoxythymidine monophosphate can be synthesised by the pathway.


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