Fig. 1

ATF3 binding profiling using isogenic HCT116 cells. a rAAV-mediated genome editing was applied to generate ATF3-knocked out HCT116 cells. rAAV-mediated homologous recombination led to insertion of the AAV targeting vector into ATF3 exon 3. A deletion of 22 bp was generated in one ATF3 allele after Cre-mediated excision of the Neo selection gene. LA and RA, left and right homology arms; ITR, inverted terminal repeat; KO, knockout. b ATF3 expression was completely abolished in ATF3-KO cells. Indicated cells were treated with 1.5 μM of CPT and subjected to Western blotting. c Venn diagram showing ATF3-binding peaks in ATF3 wild-type (ATF3-WT) and knockout (ATF3-KO) cells. d Heatmap and intensity plots showing ATF3 peaks in ATF3 WT and KO cells. e Representative genome browser views of ATF3 peaks. ATF3 peaks near ATF3, STK40, HYI, SPRY1, and UTP23 were shown for both ATF3-WT and KO cells. f, g ChIP-qPCR was used to validate ATF3 binding to representative genome sites that were referred to as the names of their annotated genes. NR, no-binding control region. Error bars represent SD for three replicate measurements. h The binding intensity determined by independent ChIP-qPCR assays was correlated with ChIP-seq scores of peaks tested in (f) and (g)