Fig. 1: Heterotypic expression of Confetti identifies polyclonal origins of Apc-deficient tumours.
From: Polyclonality overcomes fitness barriers in Apc-driven tumorigenesis
a, Schematic of experimental approach. Tam, tamoxifen. b, Immunohistochemistry for O-6-ethyl-guanine (O6-EG) in small intestinal crypts after ENU treatment. Scale bars, 25 μm. c, Jitter plot quantifying O6-EG positivity with time following ENU injection. n = 3 mice per timepoint; 7 intestinal regions scored per mouse. d, Kaplan–Meier curves for Apchet + ENU, Apchet, wild-type (WT) + ENU and wild-type mice aged until the humane endpoint. Mantel–Cox P value < 0.0001. n = 49 mice for Apchet + ENU, 10 for Apchet, 32 for wild type + ENU and 5 for wild type. e, Number of intestinal tumours per mouse under indicated conditions. n = 5 mice for Apchet + ENU, 8 for Apchet, and 20 for wild type + ENU. Two-sided Wilcoxon rank-sum tests. f, Representative wholemounts for Apchet and Apchet + ENU. S1–S5, small intestine; C1, proximal colon; C2, distal colon. Scale bars, 10 mm. g,h, Regional differences in tumour burden. n = 8 mice for Apchet (g), 5 for Apchet + ENU (h). i,j, Representative confocal micrographs showing an uncoloured tumour (i) and three examples of homotypic tumours (j). Scale bars, 200 μm. k, Frequency of Confetti labels in homotypic tumours. Counts based on 1,352 intestinal tumours. n = 5 mice. l, Confocal micrographs showing three examples of heterotypic tumours. m, Mean heterotypic fraction and regional distribution. n = 5 mice. Prox., proximal; SI, small intestine. Scale bars, 500 μm. In all box plots, the centre line shows the median, the bottom hinge shows the 25% quantile, the top hinge shows the 75% quantile, the bottom whisker shows the smallest observation greater than or equal to bottom hinge minus 1.5 × interquartile range (IQR), and the top whisker shows the largest observation less than or equal to the top hinge plus 1.5 × IQR.
