Extended Data Fig. 7: The loss of LBR and LAP2 leads to reorganisation of 3D genome topology.
a, Principal component analysis of Pico-C libraries shows clear genotype separation across replicates, relates to Fig. 7. b, Pico-C reaches sub-5 kb resolution in all genotypes (cutoff of 80% bins with minimum 1k interactions, as done in ref. 15). c, Genome-wide Pico-C contact maps reveal no large-scale genomic aberrations in DKO or TKO HCT116 cell lines. d, Representative Micro-C maps from chr18 and chrX show genome-wide changes in compartmentalization between control and TKO. e, Neighbourhood analysis in DKO for the genomic regions commonly switching compartments mirrors the trends observed in TKO (main Fig. 7d), with loci switching from B.1 to A or B.2 adopting the identity of surrounding regions. The regions under consideration are those common to DKO and TKO cell lines. f, B.1 compartments undergoing switching exhibit accompanying changes in H3K9me3 and H3K27me3 enrichment. g, Stacked bar plots showing proportion of genes within the encompassed regions switching from B.1 to A (from e) with the indicated deregulation status compared to WT HCT116 cells. P-values (one-sided Fisher’s exact test) are depicted for upregulated genes in B.1 to A regions, compared to the rest of the genome (DKO 8.36e-16; TKO 7.16e-20). h, Gene density is higher around lost B.2 loci compared to stable or gained B.2 compartments. i, Deeply sequenced Pico-C maps and chromatin profiles (ATAC-seq, CTCF, RNA-seq, H3K9me3, H3K27me3) at a representative high-NAD region reveal a contrasting trend to main Fig. 7g, with the spread of repressive histone marks upon B.2 compartment gain. LMNB1 and NAD data94; HP1α95; CTCF binding from ENCODE (UCSC Genome Browser, TFBS Clusters v3). Statistics source data are available in source data.
