Fig. 3

Meta-analysis of somatic mutation data from healthy donors defines basal and mutagen-driven mutagenesis in adult tissues. Sixty-nine single genomes from epidermis (EP), kidney tubule 1 (KT1), kidney tubule 2 (KT2), subcutaneous fat (SAT), and visceral fat (VAT) were analyzed together with public datasets of somatic mutations from WGS of clonally expanded non-cancer cells, including skin fibroblasts (SkinFB) [15]; liver, intestine, and colon stem cells [12]; skeletal muscle progenitors (SkM) [11]; and blood progenitors [13]. a tSNE plot of the trinucleotide profile of somatic SNVs. Multiple tissues displaying a common mutation profile (SkM, SAT, VAT, KT1, and blood) were named “common progenitors.” b Relative contribution of the eight mutational signatures identified in healthy cells via non-negative matrix factorization. Each signature was named after the most similar single base substitution (SBS) signature from [18]. c Average yearly increase of somatic SNVs obtained by linear fit of mutations with age in the common progenitors, KT2, liver stem cells, and intestinal stem cell (intestine and colon) groups. P values from linear mixed models are shown in Additional file 1: Table S3a. d. e Linear increase of mutations with age and signature profile of SBS5 (d) and SBS40 (e) in KT2 (red), liver (yellow), and common progenitors and intestine-derived (colon and intestine stem cells) samples (gray). SBS5 and SBS40 showed similar profiles (bottom), but different tissue distribution