Abstract:Processing of AID (activation-induced cytidine deaminase)-dependent dU:dG mismatches by the base excision repair (BER) and mismatch repair (MMR) pathways generates untemplated mutations during somatic hypermuation (SHM) or DNA breaks during class switch recombination (CSR). Genetic deletion of UNG or MSH2, which are essential for BER or MMR, respectively, impairs CSR and alters the spectrum of mutations in SHM. Ablation of both UNG and MSH2 completely blocks CSR and limits SHM to GC transition mutations. Phosp… Show more
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