ArticleNucleic acids research2026
UNG-RPA interaction governs the choice between high-fidelity and mutagenic uracil repair.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Mammalian uracil DNA glycosylase (UNG) removes uracils and initiates high-fidelity base excision repair to maintain genomic stability. During B cell development, activation-induced cytidine deaminase (AID) generates uracils in DNA, which UNG processes in an error-prone fashion to accomplish immunoglobulin (Ig) somatic hypermutation or class switch recombination (CSR). The mechanism that governs high-fidelity versus mutagenic uracil repair is not understood. The B cell tropic murine Gammaherpesvirus 68 (MHV68/MHV-4) encodes a functional homolog of UNG that can process AID-induced genomic uracils. MHV68UNG did not support hypermutation, suggesting intrinsic properties of UNG influence repair outcome. Noting the structural divergence between the UNGs, we define the RPA-interacting motif as a determinant of mutation outcome. UNG or RPA mutants unable to interact support only high-fidelity repair. In B cells, transversions at the Ig variable region are decreased, while CSR is supported. Thus UNG-RPA governs the generation of mutations and has implications for locus-specific mutagenesis in B cells and deamination-associated mutational signatures in cancer.
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