Fig. 5: Comparison of subcompartment repositioning in tumours after WGD.

a, Volcano plots of segmented genomic regions between each tumour and control cells. Selected CoREs are labelled on the basis of genes overlapping or in the proximity (±1 Mb) of the region. P values calculated using DiffComp. NS, not significant. b, Differential ChIP–seq signal in CoRE regions between control samples and each 20-weeks post-WGD tumour. c, Correlation between percentage of chromosomes affected by CoREs and CNVs for each chromosome in RPE TP53^−/− 20-weeks post-WGD tumours. d, The number of differentially expressed genes in regions unaffected (None) or affected by CNVs, CoREs or both. e, Expected and observed percentage of CoREs near to (±1 Mb) or overlapping with differentially expressed genes in the RPE TP53^−/− 20-weeks post-WGD tumours and control samples. f, Enrichment of differentially expressed genes in 20-weeks post-WGD tumours versus control in activating or inactivating CoREs. g, Normalized expression levels in single cells of selected differentially expressed genes between RPE TP53^−/− control samples and 20-weeks post-WGD tumours. h,j, Detailed characterization of the compartment and histone modification changes in the regions of chromosome 3 (h) and chromosome 2 (j) in RPE TP53^−/− control and tumour 1. Top, subcompartment assignments inferred by Calder. Bottom, histone mark intensities. i,k, Distance-normalized interaction maps at 25 kb resolution in the regions of chromosome 3 (i) and chromosome 21 (j) in RPE TP53^−/− control and tumour samples (top). Histone mark intensities for the corresponding sample (middle), significant interactions RPE TP53^−/− control and tumour 1 samples (bottom). P values calculated using HiC-DC l, Compartment rank in control, WGD and tumours for each activating and inactivating CoRE region. Lines connect compartment ranks belonging to the same CoRE region. For e and f, P values were derived by data permutation (n = 1,000).

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