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. 2020 Nov 9;11:581119. doi: 10.3389/fimmu.2020.581119

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Copyright © 2020 Mastio, Saeed, Wurzer, Krecke, Westerberg and Thomas

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Somatic hypermutation. (A) Somatic hypermutation of the immunoglobulin heavy chain is mediated by the activity of the enzyme activation-induced cytidine deaminase (AID). AID accesses nucleotides on single strand DNA (ss-DNA) during transcription of RNA e.g. by RNA polymerase II (RNA pol II). (B) AID deaminates cytidine (C) nucleotides converting them to uracil (U). This is identified as DNA damage that can be repaired by (1) transcription coupled repair where the uracil is transcribed as thymidine (T), (2) base excision repair (BER) pathway where Uracil-DNA glycosylase (UNG) detects and excises U leading to replacement by any base by the TLS polymerase and Rev1 and (3) mismatch repair (MMR) pathway where Msh2 and Msh8 identify the U and repair mismatch using error prone Pol and Exo1.