Extended Data Fig. 7: Examples of mutation patterns generated by lesion segregation from a diverse range of clinically relevant mutagens.

a–c, Genome-wide mutation asymmetry plots (shown as per Fig. 2a–c) for mutagen exposed human iPSCs⁵. Cells exposed to simulated solar radiation illustrate lesion segregation for ultraviolet damage (a). Immediately adjacent mutations (intermutation distance 10⁰) indicate CC→TT dinucleotide changes. Despite a low total mutation load (1,308 nucleotide substitutions, 842 informative T→A changes), the mutational asymmetry of lesion segregation is evident for the aristolochic acid exposed clone⁵ (b) and the polycyclic aromatic hydrocarbon DBADE (c) that is found in tobacco smoke. d, Summary mutation asymmetry ribbons (as per Fig. 2d) for all mutagen exposed clones with rl₂₀ > 5, which illustrates the independence of asymmetry pattern between replicate clones, almost universal asymmetry on chromosome X, and approximately 50% of the autosomal genome with asymmetry over autosomal chromosomes. The dominant mutation type is indicated for each mutagen. In those clones with low mutation rates, some sister exchange sites are likely to have been missed leading to reduced asymmetry signal (for example, on the X chromosome). Segments with <20 informative mutations are shown in white.