Ehrlich M, Lin F H, Ehrlich K, Brown S L, Mayo J A
J Virol. 1977 Sep;23(3):517-23. doi: 10.1128/JVI.23.3.517-523.1977.
Phage XP-12, which has complete substitution of the cytosine residues in its DNA with 5-methylcytosine residues, was shown to inhibit incorporation of uracil into host DNA and RNA during the latent period. This apparent inhibition of host macromolecular synthesis was not accompanied by extensive degradation of the host chromosome. Phage DNA synthesis in infected cells occurred at a faster rate than host DNA synthesis in analogous uninfected cells. However, phage DNA synthesis could not be accurately monitored by incorporation of [methyl-3H]thymidine into DNA because, soon after infection, there was a marked inhibition of utilization of exogenous thymidine for DNA synthesis. Phage infection conferred upon a thymine auxotrophic host the ability to synthesize thymine nucleotides for phage DNA synthesis. It is suggested that a phage-induced thymidylate synthetase activity is partially responsible for the inhibition of thymidine incorporation.
噬菌体XP - 12的DNA中的胞嘧啶残基被5 - 甲基胞嘧啶残基完全取代,研究表明,在潜伏期,它能抑制尿嘧啶掺入宿主DNA和RNA中。这种对宿主大分子合成的明显抑制并未伴随着宿主染色体的广泛降解。感染细胞中的噬菌体DNA合成比类似未感染细胞中的宿主DNA合成速率更快。然而,由于感染后不久,外源胸腺嘧啶用于DNA合成的利用率受到显著抑制,因此无法通过将[甲基 - 3H]胸腺嘧啶掺入DNA来准确监测噬菌体DNA合成。噬菌体感染赋予胸腺嘧啶营养缺陷型宿主合成胸腺嘧啶核苷酸用于噬菌体DNA合成的能力。有人认为,噬菌体诱导的胸苷酸合成酶活性部分导致了胸腺嘧啶掺入的抑制。