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. 2020 Nov 30;11:6118. doi: 10.1038/s41467-020-19961-w

Fig. 5. KAT5 depletion reduces olaparib-induced double-strand breaks and relies on the 53BP1/REV7 pathway to rescue olaparib-induced cytotoxicity.

Fig. 5

a Chromatin fractionation experiment shows that while MMS (0.01%) and olaparib (1 μM) co-treatment for 3 h induces trapping of PARP1 on the chromatin, this effect is not rescued by KAT5 depletion. An independent replicate experiment is shown in Supplementary Fig. 9a. b Neutral comet assay showing that olaparib treatment (10 μM for 24 h) induces double-strand breaks in HeLa BRCA2-knockout cells, and that this effect is abrogated by KAT5 depletion. At least 120 comets from each of two experiments were pooled for each sample. Medians are shown as horizontal bars. Asterisks indicate statistical significance (Mann–Whitney test, two-sided). c PARPi resistance caused by KAT5 depletion is dependent on 53BP1. The averages of nine experiments are shown, with standard deviations as error bars. d REV7 is required for the PARPi resistance after KAT5 knockdown. The averages of three experiments are shown, with standard deviations as error bars. Source data are provided as a Source Data file.