Warner H R, Thompson R B, Mozer T J, Duncan B K
J Biol Chem. 1979 Aug 25;254(16):7534-9.
Bacteriophage T5 induces a deoxyuridine 5'-triphosphate nucleotidohydrolase (dUTPase) activity during infection of Escherichia coli. A T5 mutant (T5 dut) unable to induce this dUTPase activity has been isolated. Although this mutant is viable, the E. coli dUTPase activity is not sufficiently active to exclude uracil from the progeny DNA and about 3% of the thymine is replaced by uracil. When the mutant is grown in an E. coli dut host about 12% of the thymine in the progeny DNA is replaced by uracil. T5 phage containing 12% uracil can replicate in uracil-DNA glycosylase-deficient (ung) hosts with high efficiency, but fail to replicate in ung+ hosts. The amount of thymine replaced by uracil in the progeny produced in dut hosts is nearly independent of the ung genotype, indicating that the host uracil-DNA glycosylase-dependent repair pathway is not operating efficiently to remove uracil from T5 progeny DNA.
噬菌体T5在感染大肠杆菌期间诱导一种脱氧尿苷5'-三磷酸核苷酸水解酶(dUTPase)活性。已分离出一种无法诱导这种dUTPase活性的T5突变体(T5 dut)。尽管该突变体是有活力的,但大肠杆菌的dUTPase活性不足以从子代DNA中排除尿嘧啶,约3%的胸腺嘧啶被尿嘧啶取代。当该突变体在大肠杆菌dut宿主中生长时,子代DNA中约12%的胸腺嘧啶被尿嘧啶取代。含有12%尿嘧啶的T5噬菌体能够在尿嘧啶-DNA糖基化酶缺陷(ung)宿主中高效复制,但在ung+宿主中无法复制。在dut宿主中产生的子代中被尿嘧啶取代的胸腺嘧啶量几乎与ung基因型无关,这表明宿主依赖尿嘧啶-DNA糖基化酶的修复途径不能有效地从T5子代DNA中去除尿嘧啶。