O'Connor T R, Boiteux S, Laval J
Groupe Réparation des Lésions Radio et Chimio Induites, UA 147 CNRS, Institut Gustave Roussy, Villejuif, France.
Nucleic Acids Res. 1988 Jul 11;16(13):5879-94. doi: 10.1093/nar/16.13.5879.
Single-stranded M13mp18 phage DNA was methylated with dimethylsulfate (DMS), and further treated with alkali to ring-open N7-methylguanine residues and yield 2-6-diamino-4-hydroxy-5N-methylformamidopyrimidine (Fapy) residues. Nucleotide incorporation during in vitro DNA synthesis on methylated template using E. coli DNA polymerase Klenow fragment (Kf polymerase) was reduced compared to the unmethylated template. Additional treatment of the methylated template with NaOH to generate Fapy residues, further reduced in vitro DNA synthesis compared to the synthesis on methylated templates, which suggested that Fapy residues were a block to in vitro DNA synthesis. Analysis of the termination products on sequencing gels, assuming that synthesis stops one base before a blocking lesion, indicated that arrest of DNA synthesis upon direct alkylation of single-stranded DNA occurred 1 base 3' to template adenine residues in the case of Kf polymerase and 1 base 3' to adenine and cystosine residues for T4 polymerase. When the alkylated templates were treated with NaOH to produce a template which converted all the N7-methylguanine residues to Fapy residues, the blocks to DNA synthesis were still observed one base before adenine residues. In addition to the stops previously observed for the methylated templates, however, new stops occurred one base 3' to template guanine residues for synthesis using both Kf polymerase and T4 polymerase. Fapy residues, therefore, represent a potential lethal lesion which may also arrest in vivo DNA synthesis if not repaired.
单链M13mp18噬菌体DNA用硫酸二甲酯(DMS)进行甲基化,然后用碱进一步处理,使N7 - 甲基鸟嘌呤残基开环,生成2 - 6 - 二氨基 - 4 - 羟基 - 5N - 甲基甲酰胺嘧啶(Fapy)残基。与未甲基化模板相比,使用大肠杆菌DNA聚合酶Klenow片段(Kf聚合酶)在甲基化模板上进行体外DNA合成时核苷酸掺入减少。用NaOH对甲基化模板进行额外处理以生成Fapy残基,与在甲基化模板上的合成相比,进一步降低了体外DNA合成,这表明Fapy残基是体外DNA合成的一个障碍。在测序凝胶上分析终止产物,假设合成在阻断损伤前一个碱基处停止,结果表明,对于Kf聚合酶,单链DNA直接烷基化后DNA合成的停滞发生在模板腺嘌呤残基3'端的1个碱基处;对于T4聚合酶,发生在腺嘌呤和胞嘧啶残基3'端的1个碱基处。当用NaOH处理烷基化模板以产生将所有N7 - 甲基鸟嘌呤残基转化为Fapy残基的模板时,在腺嘌呤残基前一个碱基处仍观察到DNA合成的阻断。然而,除了之前在甲基化模板中观察到的终止外,使用Kf聚合酶和T4聚合酶进行合成时,在模板鸟嘌呤残基3'端的1个碱基处出现了新的终止。因此,Fapy残基代表一种潜在的致死性损伤,如果不修复,也可能在体内阻止DNA合成。