Department of Biological Sciences, Ohio University, Athens, Ohio, United States of America.
Molecular and Cellular Biology Graduate Program, Ohio University, Athens, Ohio, United States of America.
PLoS One. 2024 Sep 17;19(9):e0310601. doi: 10.1371/journal.pone.0310601. eCollection 2024.
Non-enzymatic spontaneous deamination of 5-methylcytosine, producing thymine, is the proposed etiology of cancer mutational signature 1, which is the most predominant signature in all cancers. Here, the proposed mutational process was reconstituted using synthetic DNA and purified proteins. First, single-stranded DNA containing 5-methylcytosine at CpG context was incubated at an elevated temperature to accelerate spontaneous DNA damage. Then, the DNA was treated with uracil DNA glycosylase to remove uracil residues that were formed by deamination of cytosine. The resulting DNA was then used as a template for DNA synthesis by yeast DNA polymerase δ. The DNA products were analyzed by next-generation DNA sequencing, and mutation frequencies were quantified. The observed mutations after this process were exclusively C>T mutations at CpG context, which was very similar to signature 1. When 5-methylcytosine modification and uracil DNA glycosylase were both omitted, C>T mutations were produced on C residues in all sequence contexts, but these mutations were diminished by uracil DNA glycosylase-treatment. These results indicate that the CpG>TpG mutations were produced by the deamination of 5-methylcytosine. Additional mutations, mainly C>G, were introduced by yeast DNA polymerase ζ on the heat-damaged DNA, indicating that G residues of the templates were also damaged. However, the damage on G residues was not converted to mutations with DNA polymerase δ or ε.
5-甲基胞嘧啶的非酶促自发脱氨产生胸腺嘧啶,这被认为是癌症突变特征 1 的病因,该特征是所有癌症中最主要的特征。在这里,使用合成 DNA 和纯化的蛋白质重新构建了提议的突变过程。首先,将含有 CpG 环境中 5-甲基胞嘧啶的单链 DNA 在高温下孵育,以加速自发的 DNA 损伤。然后,用尿嘧啶 DNA 糖基化酶处理 DNA,以去除由胞嘧啶脱氨产生的尿嘧啶残基。然后将得到的 DNA 用作酵母 DNA 聚合酶 δ 的 DNA 合成模板。通过下一代 DNA 测序分析 DNA 产物,并定量突变频率。在这个过程之后观察到的突变仅为 CpG 环境中的 C>T 突变,这与特征 1 非常相似。当 5-甲基胞嘧啶修饰和尿嘧啶 DNA 糖基化酶都被省略时,在所有序列环境中 C 残基上都会产生 C>T 突变,但这些突变在尿嘧啶 DNA 糖基化酶处理后减少。这些结果表明 CpG>TpG 突变是由 5-甲基胞嘧啶的脱氨产生的。额外的突变,主要是 C>G,由热损伤 DNA 上的酵母 DNA 聚合酶 ζ 引入,表明模板上的 G 残基也受到了损伤。然而,G 残基上的损伤不能通过 DNA 聚合酶 δ 或 ε 转化为突变。