Extended Data Fig. 5: RAD21 depletion-induced translocations are associated with DNA replication.
From: Cohesin maintains replication timing to suppress DNA damage on cancer genes
a Representative profile of translocation junction bias in IAA-treated WT and RAD21-mAC K562 cells from TP53 locus. The legends of indicated panels are described in Fig. 4a. b The correlation between PEM-seq-identified translocation junction bias and Okazaki fragments from OK-seq. Each point indicates a unique peak within regions displayed in Fig. 4a or Extended Data Fig. 5a. The two-sided Pearson’s correlation coefficients (PCC) and p-values (p) are marked. The grey shadow indicates 95% confidence interval of a linear regression model. c Percentages of genome-wide translocation junctions within the Watson or Crick peaks. Mean ± SD from three biological replicates; two-sided t-test; *, p < 0.05; **, p < 0.01; ***, p < 0.001. d Orientations of PEM-seq-captured translocation and Okazaki fragments. The leftward fork contains Okazaki fragments on the Watson strand. DNA breaks occurring on either the template DNA of leading or lagging strands lead to the translocation junctions with a positive or Watson orientation. The rightward fork contains Okazaki fragments on the Crick strand and DNA breaks on the leading or lagging strand form translocation junctions with a negative or Crick orientation. e Representative profile of PEM-seq-captured translocations in K562 cells under HU or APH treatment.
