碱基类似物在人细胞的前导链与滞后链模板上诱导的大片段缺失和非靶向替换。
Large deletions and untargeted substitutions induced by abasic site analog on leading versus lagging strand templates in human cells.
机构信息
Graduate School of Biomedical and Health Sciences, Hiroshima University, Minami-ku, Hiroshima, Japan.
Biotechnology Research Institute for Drug Discovery, National Institute of Advanced Industrial Science and Technology, Higashi, Tsukuba, Ibaraki, Japan.
出版信息
Mutagenesis. 2019 Dec 19;34(5-6):421-429. doi: 10.1093/mutage/gez034.
The tetrahydrofuran-type abasic site analog (THF) induces large deletion mutations in human cells. To compare the large deletions induced by THF on leading and lagging strand templates, plasmid DNAs bearing the analog at a specific position outside the supF gene were introduced into human U2OS cells. The replicated DNAs recovered from the transfected cells were electroporated into an Escherichia coli indicator strain. THF on the lagging strand template produced more supF mutants than THF on the leading strand template. This unequal mutagenicity was due to the higher frequencies of not only large deletions but also untargeted base substitutions induced in the gene. These results suggested that both types of mutations occur more frequently when abasic sites are formed on the lagging strand template.
四氢呋喃型无碱基位点类似物（THF）可在人细胞中诱导大片段缺失突变。为了比较 THF 在前导链和滞后链模板上诱导的大片段缺失，将含有该类似物的质粒 DNA 引入人 U2OS 细胞中，该类似物位于 supF 基因之外的特定位置。从转染细胞中回收的复制 DNA 被电穿孔到大肠杆菌指示菌株中。滞后链模板上的 THF 比前导链模板上的 THF 产生更多的 supF 突变体。这种不等效诱变是由于不仅在基因中诱导了更高频率的大片段缺失，而且还诱导了非靶向碱基取代。这些结果表明，当无碱基位点形成在滞后链模板上时，这两种类型的突变发生得更频繁。
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