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. Author manuscript; available in PMC: 2019 Apr 16.
Published in final edited form as: Cell Rep. 2018 Jul 24;24(4):883–894. doi: 10.1016/j.celrep.2018.06.091

Figure 2: Evidence of UV damage in iPSCs.

Figure 2:

(A, B) Plots showing the percentage of mutations in each of the 96 substitution classes defined by the substitution type and one base sequence context immediately 3’ and 5’ to the mutated base. (A) Example iPSC line with UV damage (sample 3_1); (B) Example of iPSC line without UV damage (72_1). (C) Heatmap showing the correlation between the mutational profiles of the 18 iPSC lines and 30 mutational signatures derived from 40 tumor types (Alexandrov et al., 2013b). The number of SNVs, CC>TT DNVs and CNAs are shown. (D) Distribution of SNV types in each of the 18 iPSC lines. (E) The fraction of all mutations in each of the 18 iPSC lines that are DNVs. Eight iPSC lines have a high incidence of CC>TT DNVs (4.8% of all point and indel mutations in the eight most mutated iPSC lines), while the number of the other DNVs is low and constant in all 18 iPSCs (0.4–1.2% of all somatic mutations). See also Figure S2, Table S5.