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首页> 外文期刊>Biochemistry >The Mutagenicity of Thymidine Glycol in Escherichia coli Is Increased When It Is Part of a Tandem Lesion
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The Mutagenicity of Thymidine Glycol in Escherichia coli Is Increased When It Is Part of a Tandem Lesion

机译：当它是串联病变的一部分时，胸苷乙二醇在大肠杆菌中的致突变性增加。

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Tandem lesions are comprised of two contiguously damaged nucleotides. Tandem lesions make upnthe major family of reaction products generated from a pyrimidine nucleobase radical, which are formed innlarge amounts by ionizing radiation. One of these tandem lesions contains a thymidine glycol lesion flankednon its 50-side by 2-deoxyribonolactone (LTg). The replication of this tandem lesion was investigated innEscherichia coli using single-stranded genomes. LTg is a much more potent replication block than thymidinenglycol and is bypassed only under SOS-induced conditions. The adjacent thymidine glycol does notnsignificantly affect nucleotide incorporation opposite 2-deoxyribonolactone in wild-type cells. In contrast,nthe misinsertion frequency opposite thymidine glycol, which is negligible in the absence of 2-deoxyribonolactone,nincreases to 10% in wild-type cells when LTg is flanked by a 30-dG. Experiments in which the flankingnnucleotides are varied and in cells lacking one of the SOS-induced bypass polymerases indicate that thenmutations are due to a mechanism in which the primer misaligns prior to bypassing the lesion, which allowsnfor an additional nucleotide to be incorporated across from the 30-flanking nucleotide. Subsequentnrealignment and extension results in the observed mutations. DNA polymerases II and IV are responsiblenfor misalignment induced mutations and compete with DNA polymerase V which reads through the tandemnlesion. These experiments reveal that incorporation of the thymidine glycol into a tandem lesion indirectlyninduces increases in mutations by blocking replication, which enables the misalignment-realignmentnmechanism to compete with direct bypass by DNA polymerase V.
机译：串联损伤由两个连续受损的核苷酸组成。串联损伤构成了由嘧啶核碱基自由基产生的主要反应产物家族，其通过电离辐射大量形成。这些串联损伤之一包含在其50侧带有2-deoxyribonolactone（LTg）的胸苷乙二醇损伤。使用单链基因组在大肠杆菌中研究了这种串联病变的复制。 LTg是比胸苷二醇更有效的复制阻滞剂，仅在SOS诱导的条件下才被旁路。相邻的胸苷二醇对野生型细胞中与2-脱氧核糖内酯相反的核苷酸掺入没有显着影响。相反，当LTg与30 dG侧接时，在没有2-脱氧核糖内酯的情况下，与胸苷二醇相对的误插入频率可以忽略不计，增加到10％。侧翼核苷酸发生变化并且在缺少一种SOS诱导的旁路聚合酶的细胞中进行的实验表明，突变是由于一种机制，在这种机制中，引物在绕过病变之前会发生错位，从而允许从30个核苷酸中引入另外的核苷酸-侧翼核苷酸。随后的重排和延伸导致观察到的突变。 DNA聚合酶II和IV负责错位诱导的突变，并与DNA聚合酶V竞争，而V酶则读取遍及腺的位置。这些实验表明，将胸苷二醇掺入串联病变中可通过阻断复制而间接诱导突变的增加，从而使错位-重排列机制能够与DNA聚合酶V的直接旁路竞争。

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