Fig. 3: ID4 SSTR and MH mutations are increased genome-wide in RNase-H2-deficient RPE-1 cells.
From: Signatures of TOP1 transcription-associated mutagenesis in cancer and germline
a, Schematic of the mutation-accumulation experiment. Long-term culture of hTERT RPE-1 TP53−/− RNase-H2-wildtype (WT) and RNase-H2-null cell lines (RNASEH2A-KO (AKO), RNASEH2B-KO (BKO)) bottlenecked every 25 doublings by single-cell sorting. b, Mutations acquired during long-term culture were significantly enriched for 2–5 bp deletions in RNase-H2-null cells, but the other mutation categories were not (Extended Data Fig. 4e). Data are mean ± s.d. Statistical analysis was performed using two-sided Fisher’s exact tests with Bonferroni correction, comparing wild type (counts pooled from n = 3 independent clones) versus KO (n = 2 independent clones) for 2–5 bp deletions versus all of the other indel types. c, d, ID4 occurs in RNase-H2-null cells (c) and is the major signature after subtracting background mutations that are observed in wild-type cells (d).
