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. 2019 Dec 24;5(12):e03057. doi: 10.1016/j.heliyon.2019.e03057

Figure 2.

Figure 2

Replication stress-associated DSBs are repaired through a PolQ-mediated repair pathway with terminating HR in MMR-proficient cells. (A–D) HCT116 cells were treated with HU, as shown in the workflow (A). The statuses of HR were determined by the intensities of p-Rad51 and pp-Rad51 signals (A,B). Signals observed PolQ dependent decay are pointed by red arrowheads (A). Source images of blots are shown in Supplementary Fig. 2. p- and pp-Rad51 signals normalized with β-Actin signal are shown (B). DSB statuses were determined by the merged foci of γH2AX and 53BP1 (C,D). Representative images are shown (C). The numbers of 53BP1 foci in each cell were plotted (n numbers and P values are indicated in graph) (D). Two-tailed Welch's t-test was used for statistical analysis. (E,F) Rad51 accumulation status were determined together with the damage status that was determined by γH2AX signal after cells were treated as in the workflow (E). Source images of blots are shown in Supplementary Fig. 3. Rad51 and γH2AX signals normalized with histone H3 signal are shown (F). Error bars represent ±SD.