Somatic hypermutation:: activation-induced deaminase for C/G followed by polymerase η for A/T
Somatic hypermutation:: activation-induced deaminase for C/G followed by polymerase η for A/T
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DOI：
10.1084/jem.20062409
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发表时间：
2007-01-22
影响因子：
15.3
通讯作者：
Rada, Cristina
中科院分区：
文献类型：
--
作者：
Neuberger, Michael S.;Rada, Cristina
体细胞超突变 (SHM) 将核苷酸替换引入免疫球蛋白可变 (Ig V) 区基因的所有四个碱基，但 C/G 和 A/T 对的突变是通过不同的机制实现的。 C/G 对突变是激活诱导脱氨酶 (AID) 催化的 C → U 脱氨作用的直接结果。然而，A/T 对的突变需要在 AID 生成的 U/G 不匹配的补丁修复过程中发生第二个诱变过程。几种 DNA 聚合酶被认为在 SHM 中发挥作用，但越来越多的证据表明 A/T 处的突变绝大多数是通过招募 DNA 聚合酶 eta 来实现的。
Somatic hypermutation (SHM) introduces nucleotide substitutions into immunoglobulin variable (Ig V) region genes at all four bases, but the mutations at C/G and A/T pairs are achieved by distinct mechanisms. Mutations at C/G pairs are a direct consequence of the C -> U deamination catalyzed by activation-induced deaminase ( AID). Mutations at A/T pairs, however, require a second mutagenic process that occurs during patch repair of the AID-generated U/G mismatch. Several DNA polymerases have been proposed to play a role in SHM, but accumulating evidence indicates that the mutations at A/T are overwhelmingly achieved by recruitment of DNA polymerase eta.