Extended Data Fig. 5: TP53 loss is not the cause of LCS.
From: Whole-genome doubling drives oncogenic loss of chromatin segregation
a, Ratios of inter-chromosomal contact enrichments (observed vs. expected) between TP53−/− and TP53 WT samples for CP-A and RPE cells. Chromosomes were sorted by length. Long chromosomes (chr1 to chr14 and chrX) and short chromosomes (chr15 to chr22) are highlighted. p-values are calculated by two-tailed Wilcoxon test. b, Heatmap of ratios of genomic bins belonging to the indicated sub-compartments that gain vs. lose contacts between TP53−/− and TP53 WT samples for CP-A and RPE cells. c, Boundary insulation scores in TP53 WT and TP53−/− for CP-A and RPE samples. Only boundaries shared between the two conditions are considered. b-c p-values calculated by two-tailed Wilcoxon test. d, Representative image of immunoblot (above) and quantification (below) of CTCF protein expression in TP53 WT and TP53−/− CP-A (left) and RPE (right) cells (n = 1 experiment). e, CTCF mRNA expression levels in RPE and CP-A TP53 WT cell lines after treatment with 3 µM doxorubicin (n = 2 independent experiments).
