Figure 1.

Current model of somatic hypermutation (based on ref. 123). Activation-induced cytidine deiminase (AID)-mediated deamination of cytidines at immunoglobulin genes results in U : G mispairs. DNA replication over uracils will promote transition mutations (C/G to T/A). Uracil can also be repaired in an error-free fashion by either base excision repair (BER) or mismatch repair (MMR). If uracils are recognized by uracil-N-glycosylase 1 (UNG) in the context of DNA replication however, abasic sites would be repaired by REV1 and other translesion polymerases leading to both transition and transversions at C : Gs. Following replication, U : G mismatches or abasic sites would engage the activity of polymerase η (pol η) resulting in mutations primarily at A : T pairs.