ArticleNature communications2025
Tissue-specific mutagenesis from endogenous guanine damage is suppressed by Polκ and DNA repair.
Article in Nature communications, 2025. 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
Knowledge of mutational patterns has expanded significantly, but linking these patterns to specific molecular mechanisms or sources of endogenous DNA damage remains challenging. Translesion synthesis (TLS) is a key determinant of mutagenesis, yet the endogenous lesions that require TLS and how TLS polymerases shape mammalian mutational landscapes are unclear. Here, we characterize somatic mutational patterns across mouse tissues deficient in the TLS polymerase Polκ and find that Polκ suppresses a distinct tissue-specific mutational signature in the liver and kidney. This signature, enriched for C > A/G/T mutations with strong transcriptional-strand bias, indicates that Polκ performs error-free bypass of endogenous guanine adducts. Nucleotide excision repair (NER) acts in parallel, mitigating some of this damage. Targeted adductomics and biochemical analyses identify endogenous N
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