Extended Data Fig. 2: Associations between soL1R burden and other genomic features of clones.

a, Linear regression between the average number of endogenous point mutations in the colorectal clones and the age of sampling in 19 individuals. Blue line represents the regression line (44.6 point mutations per year), and shaded areas indicate its 95% confidence interval. The rate is consistent with the rate previously estimated in the colon (43.6 mutations per year from Lee-Six et al., Ref. ⁵¹). b,c, Comparison of the average number of soL1Rs per individual across sex (b) and anatomical ___location of the colorectal crypts (c) in 19 individuals with normal colorectal clones with two-sided Wilcoxon rank-sum test. Box plots illustrate median values with interquartile ranges (IQR) with whiskers (1.5 x IQRs). ns, not significant. d–i, Relationship between the number of soL1R for each colorectal clone and the number of somatic point mutations (d), telomere length (e), the number of somatic SBS1 SNVs (f, clock-like mutations by deamination of 5-methylcytosine), the number of somatic SBS5+SBS40 SNVs (g, clock-like mutations by unknown process), the number of somatic SBS18 SNVs (h, possibly damage by reactive oxygen species), and the number of somatic SBS88 SNVs (i, damage by colibactin from pks+ E. coli). No obvious association was found. j, Number of LCM-based patches with various numbers of soL1Rs across different organs. LCM, laser-capture microdissection.