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首页> 外文期刊>Biochemistry >Replication of an oxidized abasic site in Escherichia coli by a dNTP-stabilized misalignment mechanism that reads upstream and downstream nucleotides
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Replication of an oxidized abasic site in Escherichia coli by a dNTP-stabilized misalignment mechanism that reads upstream and downstream nucleotides

机译：通过读取上游和下游核苷酸的dNTP稳定错位机制在大肠杆菌中复制氧化的无碱基位点

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Abasic sites (AP) and oxidized abasic lesions are often referred to as noninstructive lesions because they cannot participate in Watson-Crick base pairing. The aptness of the term noninstructive for describing AP site replication has been called into question by recent investigations in E. coli using single-stranded shuttle vectors. These studies revealed that the replication of templates containing AP sites or the oxidized abasic lesions resulting from C1'- (L) and C4'-oxidation (C4-AP) are distinct from one another, suggesting that structural features other than Watson-Crick hydrogen bonds contribute to controlling replication. The first description of the replication of the abasic site resulting from formal C2'-oxidation (C2-AP) is presented here. Full-length and single-nucleotide deletion products are observed when templates containing C2-AP are replicated in E. coli. Single nucleotide deletion formation is largely dependent upon the concerted effort of pol II and pol IV, whereas pol V suppresses frameshift product formation. Pol V utilizes the A-rule when bypassing C2-AP. In contrast, pol II and pol IV utilize a dNTP-stabilized misalignment mechanism to read the upstream and downstream nucleotides when bypassing C2-AP. This is the first example in which the identity of the 3'-adjacent nucleotide is read during the replication of a DNA lesion. The results raise further questions as to whether abasic lesions are noninstructive lesions. We suggest that abasic site bypass is affected by the local biopolymer structure in addition to the structure of the lesion.
机译：无碱基位点（AP）和氧化的无碱基位病变通常被称为非指导性病变，因为它们不能参与Watson-Crick碱基配对。近期使用单链穿梭载体在大肠杆菌中进行的研究已经质疑非指导性术语用于描述AP位点复制的适用性。这些研究表明，包含AP位点或C1'-（L）和C4'-氧化（C4-AP）导致的氧化无碱基损伤的模板的复制彼此不同，表明除Watson-Crick氢以外的结构特征键有助于控制复制。这里介绍了由形式C2'-氧化（C2-AP）导致的无碱基位点复制的第一个描述。当含有C2-AP的模板在大肠杆菌中复制时，观察到全长和单核苷酸缺失产物。单核苷酸缺失的形成很大程度上取决于pol II和pol IV的共同努力，而pol V抑制移码产物的形成。 Pol V在绕过C2-AP时会利用A规则。相比之下，pol II和pol IV在绕过C2-AP时利用dNTP稳定的错位机制读取上游和下游核苷酸。这是第一个实例，其中在DNA损伤的复制过程中读取了3'相邻核苷酸的身份。结果进一步引起了关于无基础病变是否为非指导性病变的疑问。我们建议除病变部位的结构外，无碱基位点旁路还受局部生物聚合物结构的影响。

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