a) Gene ontology analysis of genes assigned to PC1 (n=945 genes) and PC2 (n=599 genes). b) Robust K-means clustering (PAM) of differentially expressed genes in the serum-to-2i and the reverse transition (left part). Heatmap showing enrichment of genes assigned to each K-means cluster in different stages of pre-implantation embryos (right part). N number indicated in the panel represents genes. c) Schematic representation of the cHiC analysis for the 340,000 pairwise interactions. Interactions were constrained to have a regulatory element (ATAC-seq peak or CTCF binding site) within 2 kb of both interaction anchors. The interaction network, constrained to interacting regulatory elements, contained ~135,000 distinct pairwise interactions. d) The promoter interaction intensity (sum of reads of all interactions with that promoter) in our cHiC data is in good agreement with published promoter capture in serum ESCs, n=11,842 promoters, R-values represent Pearson’s correlation coefficient. e) ChromHMM-based segmentation of the mouse genome using six chromatin states revealed CTCF binding sites, weak- and strong regulatory elements, H3K27me3-marked regions and actively transcribed gene bodies. The other state has none of the studied marks. f) Assignment of each interacting anchor site to corresponding ChromHMM states. Sites within 2 kb of a TSS were assigned as promoters. Promoter regions with H3K27me3 are colored in yellow. Strong and weak distal elements were combined and assigned as enhancers. g) Pairwise combinations of anchors assigned to one of the main chromatin states: CTCF, weak-element, strong-element or H3K27me3 region located in promoter or distal sites. Circle sizes correspond to numbers of interactions and colors represent the interaction intensities. In a-b FDR was computed using Hypergeometric tests with Benjamini-Hochberg correction.