Abstract
A mutant of Escherichia coli, tdk 32, defective for deoxythymidine kinase (ATP: thymidine 5'-phosphotransferase EC 2.7.1.21[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 [3H]-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 tdk 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 (tk) linked to rI. T4tk mutant-infected tdk 32 cells fail to incorporate [3H]-thymidine or 5-bromodeoxyuridine into DNA and the latter property formed the basis for the selection of the phage mutants. The T4tk gene is non-essential for growth both in wild type and tdk mutant cells since deoxythymidine monophosphate can be synthesised by the de novo pathway.