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Significance The somatic hypermutation of immunoglobulin (Ig) genes is usually required to make antibodies that protect us from foreign and toxic substances. This mutational process is mediated by activation-induced deaminase (AID) and is targeted to the variable (V) part of the Ig genes that encode the antigen-binding site of antibody molecules, leading to higher affinity and more effective antibodies. AID acts on single-stranded DNA that is created during the transcription of the V region. Here, we show that multiple factors that are involved in the release, from pausing to elongation of transcription, contribute to the hypermutation process, supporting the likelihood that transcriptional pausing and elongation make V region single-stranded DNA available to AID-induced mutations.

Role of Dot1L and H3K79 methylation in regulating somatic hypermutation of immunoglobulin genes