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A.T碱基对处的体细胞高频突变:聚合酶错误与dUTP掺入

Somatic hypermutation at A.T pairs: polymerase error versus dUTP incorporation.

作者信息

Neuberger Michael S, Di Noia Javier M, Beale Rupert C L, Williams Gareth T, Yang Zizhen, Rada Cristina

机构信息

Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.

出版信息

Nat Rev Immunol. 2005 Feb;5(2):171-8. doi: 10.1038/nri1553.

Abstract

Somatic hypermutation of immunoglobulin genes occurs at both C.G pairs and A.T pairs. Mutations at C.G pairs are created by activation-induced deaminase (AID)-catalysed deamination of C residues to U residues. Mutations at A.T pairs are probably produced during patch repair of the AID-generated U.G lesion, but they occur through an unknown mechanism. Here, we compare the popular suggestion of nucleotide mispairing through polymerase error with an alternative possibility, mutation through incorporation of dUTP (or another non-canonical nucleotide).

摘要

免疫球蛋白基因的体细胞超突变发生在C.G对和A.T对。C.G对的突变是由激活诱导的脱氨酶(AID)催化C残基脱氨形成U残基而产生的。A.T对的突变可能在AID产生的U.G损伤的补丁修复过程中产生,但它们通过未知机制发生。在这里,我们将通过聚合酶错误进行核苷酸错配这一普遍观点与另一种可能性,即通过掺入dUTP(或另一种非规范核苷酸)进行突变进行比较。

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