Fig. 3: Depletion of NFIB alters chromosome contacts/compartments and replication profile.
From: NFIB facilitates replication licensing by acting as a genome organizer
a Left: Heatmap of NS-seq signals in NFIB-depleted versus control U2OS cells. The fold change cutoff of signal intensity was set to 1.2. S1, peak signals decreased; S2, peak signals increased; S3, peak signals unaltered. Right: Heatmap of NS-seq signal distribution surrounding N1 peaks in NFIB-depleted versus control U2OS cells. b Different time points of synchronized NFIB-depleted U2OS cells were analyzed by Repli-seq. Control or NFIB-depleted U2OS cells were synchronized via thymidine/aphidicolin block followed by release for 0.5 h, 4 h, or 6 h to enrich cells in the early, middle, or late S phase, respectively. Graph showing the replication timing of NFIB-associated active origins (S1 peaks overlapped with N1 peaks, S1.N1, n = 415), other S1 peaks (S1.non-N1, n = 14,203), S2 peaks (n = 24,410) and total NS-seq peaks (all, n = 48,273). c Comparison between replication initiation patterns after NFIB was depleted in U2OS cells. Genome tracks showing the signals of Repli-seq, NFIB ORC1, and H3K4me3 at selected regions of chromosome 5. d Scatter plot of PC1 eigenvector of G1/S boundary or S phase U2OS cells without (shCTR) or with NFIB depletion (shNFIB) for each 250 kb genome bin. Red points: changed regions. Black points: unchanged regions. e Histogram showing the number of regions (250 kb bin) where the PC1 eigenvector significantly changed. f Knight-Ruiz (KR) balanced Micro-C contact map of chromosome 1: 162 to 183 Mb at a 100-kb resolution. g Violin plot showing the distribution of N1 peaks in different chromatin regions in G1/S phase (bin size 250 kb).
